Chronic Facial Pain in the Female Patient: Treatment Updates

Oral Maxillofacial Surg Clin N Am 19 (2007) 245–258

Chronic Facial Pain in the Female Patient: Treatment Updates Franci Stavropoulos, DDSa,*, Barbara A. Hastie, PhD, MAb a Department of Oral and Maxillofacial Surgery and Diagnostic Sciences, College of Dentistry, University of Florida, Box 100416, 1600 SW Archer Rd., Room D7-6, Gainesville, FL 32610, USA b Department of Community Dentistry & Behavioral Science, College of Dentistry, University of Florida, PO Box 103628, Gainesville, FL 32610, USA

Pain is defined as ‘‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage’’ [1]. Many individuals report pain for which there is no evident organic etiology, and it is often attributed to psychological reasons in a perfunctory fashion without full knowledge of the biopsychosocial influences of chronic pain. Pain is well established as the primary reason why people seek medical and dental care, far more frequently than seeking care for the prevention of illness or disease. The 1985 Nuprin Pain Study found that most Americans had experienced physical pain in the last 12 months and that they experienced three to four different kinds of pain every year [2]. The most frequently reported types of pain were headache, backache, and muscle, joint, stomach, menstrual, and dental pain [3]. Two decades later, similar trends were reported in nonclinical community samples, with prevalence and severity of greater impact among minorities and the elderly [4–7]. Although most of the community studies report acute pain incidences, chronic pain prevalence is more pervasive and debilitating, accounting for more than $1 billion annually in lost wages, hospitalizations, and health care expenses. The work of Dr. Hastie is supported by NIH grants NS55094, NS42754-S and as a Health Disparities Scholar of the National Center on Minority Health and Health Disparities. * Corresponding author. E-mail address: [email protected]fl.edu (F. Stavropoulos).

Acute pain serves a protective function by warning the body of pending danger, whereas chronic pain is pain that persists beyond a reasonable amount time of healing for a specific disease or injury. The cause of chronic pain is often elusive and may result in ineffective surgical intervention and ultimately the diminution of mental and physical performance. Among the most common chronic pain conditions is orofacial pain. Orofacial pain refers to a large group of disorders including temporomandibular disorders (TMDs), headaches, neuralgia, pain developing in dental or mucosal tissues, and idiopathic pain [8,9]. Notably, odontogenic pain is the most commonly reported orofacial pain. Chronic orofacial pain is often an ill-understood group of conditions for which an unclear and confounding classification exists. Orofacial pain is challenging to diagnose because of the complex anatomy of the head and neck, diverse etiologies, unpredictable pain referral patterns, presenting symptoms, and a lack of consensus regarding differential diagnostic criteria [10,11]. Unfortunately, descriptions of disorders and treatment may be influenced by the background and gender of the specialist assessing the disorder. For instance, a patient seeking care for orofacial pain from a maxillofacial surgeon may have symptoms described relative to the temporomandibular joint. On the other hand, the same patient seeking care from an otolaryngologist may be diagnosed using Costen’s outdated notion that orofacial pain is caused by missing posterior dentition [12]. Chronic orofacial pain affects approximately 10% of adults and up to 50% of the elderly

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population [9], although some epidemiologic studies have reported higher prevalence. Lipton and colleagues [13] reported that 22% of the US population experienced orofacial pain on more than one occasion in a 6-month period. Evidence exists that sex differences in masticatory muscle pain and tenderness develop as early as age 19 [14]. Women of reproductive age, with a concentration of women in their 40s, more frequently seek treatment for orofacial pain compared with men by a 2:1 ratio [15,16]. This finding is consistent with other pain conditions for which women are more likely than men to seek treatment, including headaches, fibromyalgia, autoimmune rheumatic disorders, chronic fatigue, orthopedic complaints, and irritable bowel syndrome [16–18]. Women experience more symptoms of recurrences and more intense pain [19]. There is substantial interindividual variation in the experience and response to pain; such differences are determined by the confluence of genetics and psychological and psychosocial influences. The literature is replete with experimental laboratory evidence in animals and humans and clinical evidence to explain gender differences in pain [20–26]. A seminal review by Fillingim and Maixner [27] evaluating experimental pain studies involving psychophysical designs (eg, the relationship between the physical properties of a pain stimulus and the sensory and behavior responses by the subject) concluded that in general, women exhibit greater sensitivity to laboratory pain compared with men. This finding was further substantiated through a meta-analysis conducted by Riley and colleagues [28], which found that women generally show lower pain thresholds and tolerances than men to various noxious stimuli. Effect sizes for pain threshold and tolerance range varied in magnitude and the type of pain assayed, however. Overall, ratings of experimentally induced pain show a gender disparity, with women generally reporting lower pain thresholds and tolerance than men. These reported differences are small, however, and may be inconsistently observed because of the methodology used and the numerous variables that influence pain reporting in the laboratory setting [15]. Over the past decade, significant attention has been directed to the fact that women and men have different biologic processes associated with genetic variations, growth and development, and maturation. For example, boys and girls undergo puberty and the associated effects of hormones at a similar timeframe. In girls, however, these

hormonal effects are long-lasting, including monthly menstrual cycles, perimenopause, and menopause. Gonadal hormones have been found to contribute to the variation in pain perception in several conditions. Experimental pain perception varies across the menstrual cycle in healthy women, with the greatest pain sensitivity occurring perimenstrually [29]. The severity of many pain disorders, including orofacial pain, headaches [30], and myofacial pain [31], fluctuates with the menstrual cycle, and various medical conditions, such as rheumatoid arthritis and other autoimmune diseases [32,33], may be exacerbated. For example, headache symptoms increase in approximately 60% of patients who have migraines during the premenstrual phase of their cycle, and 14% of women with migraine headaches experience headaches with menses only [30]. Even more poignant evidence exists for the relationship of gonadal hormones and pain response. Women who take estrogen replacement therapy may find their migraine symptoms worsened during menopause [34,35] or may be at increased risk for developing temporomandibular disorders [36] and back pain [37]. Women who were taking hormone replacement therapy reported more severe orofacial pain compared with individuals who were not taking hormone replacement therapy [38]. This evidence suggests that endogenous and exogenous hormones influence pain responses in women. Gender-related differences in opioid analgesia recently were examined in experimental settings in humans and nonhumans [25,29,39–41]. Studies in humans have shown conflicting evidence on whether men and women differ in their response to various classes of opioids. These differences may be caused by variations in pain assays across studies and the class of opioid examined rather than a lack of pure differences in biologic processes across genders. Considerable evidence of sex differences in pain perception has accumulated, and more recent findings suggest that women and men may differ in their responses to analgesic medications [42–44]. Although these results vary across studies [23], Fillingim and colleagues [45] reported that pentazocine, an agonist-antagonist opioid, produced quantitatively similar analgesia between the sexes. In contrast, with regard to mu opioids, specifically morphine and postoperative pain, research has shown evidence of greater analgesia among women [46,47], greater analgesia among men [48], and comparable analgesia across sexes [49]. For mu opioids, the evidence is less compelling for

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one sex or the other. Laboratory studies have demonstrated more robust analgesic responses to mu opioid agonists (eg, morphine, hydromorphone) among women compared with men [50–52]. After oral surgery, women showed greater analgesic responses to kappa-agonist-antagonist medications (eg, pentazocine, nalbuphine, and butorphanol) [49,53–55]. Fillingim and colleagues [45] reported no sex differences in the effects of pentazocine (a kappa agonist-antagonist) on experimental pain responses, however. In contrast to the relatively consistent findings regarding baseline pain perception, whereby women exhibit lower threshold and tolerance, sex differences in opioid analgesic responses vary considerably across studies. New advances in research have begun to investigate the influence of genetic factors in moderating sex differences in analgesic response. Genetic factors There has been increased attention and enhanced investigation in translational research of the role of genes and pain. Mogil and Fillingim were among the first to conduct translational studies from rodents to humans in detecting genetic variants that may influence pain perception and corresponding analgesic response [41,56]. Specifically, the Melanacortin-1 (Mc1r in rodents and MC1R in humans) gene has been shown to affect pain sensitivity and M6G (a metabolite of morphine) analgesia in mice and humans. Mogil and colleagues [41,56,57] confirmed the use of cross-species translational strategies in pharmacogenetics. Fillingim [58], Hastie [59], and others [60,61] have reported the influence of the A118G rare allele of the mu opioid receptor (OPRM1) on experimental pain perception in humans. Other genetic examination has involved the delta opioid receptor (OPRD1) and catechol O-methyltransferase, transient receptor potential A subtype 1 (TRPA1), M subtype 8 (TRPM8), V subtype 1 (TRPV1), delta opioid receptor subtype 1 (OPRD1), and fatty acid amide hydrolyase [62– 68] but has been used mostly in experimental, nonclinical settings. With regard to OPRM1 and the variant allele, A118G, Fillingim and colleagues [58] showed a sex by genotype interaction for heat pain ratings such that the rare allele was associated with lower pain ratings among men but higher pain ratings among women. These data indicate an association of a common single nucleotide polymorphism of OPRM1 with mechanical pain responses and the

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theory that this genotype may be associated with heat pain perception in a sex-dependent manner. Other investigators have reported associations of rare alleles and analgesic response, but they also have been in experimental settings [69,70] until recently, when associations have been shown with response to opioids [71–73]. These investigations are of particular importance because opioids play important roles in the clinical management of pain and the mu opioid receptor is the primary site of action for the most commonly used opioids, including morphine, fentanyl, and methadone [64]. The A118G variant receptor binds beta-endorphin, an endogenous opioid that activates the mu opioid receptor, approximately three times more tightly than the most common allelic form of the receptor. Beta-endorphin is approximately three times more potent at the A118G variant receptor than at the most common allelic form in agonist-induced activation of G proteincoupled potassium channels. Researchers have shown that single nucleotide polymorphisms in the mu opioid receptor gene can alter binding and signal transduction in the resulting receptor and may have implications for normal physiology, therapeutics, and vulnerability to develop or provide protection from diverse diseases [64]. Recently, investigators have revealed compelling evidence as to the relationship of genetics, pain, and the potential interactive affects on risk of developing chronic pain conditions, such as TMD. Although TMDs are covered in a separate article, it bears noting that Diatachenko and colleagues [74] discovered three genetic variants (eg, haplotypes) from the catechol-O-methyltransferase gene that influence pain sensitivity and the risk of developing TMD. The three haplotypesd low, average, and high pain sensitivity, respectivelyddemonstrated varied levels of association with developing chronic pain. For example, the presence of even a single haplotype, such as the low pain sensitivity, diminishes by as much 2.4 the risk of developing TMD. Conversely, the incidence rate of TMD was more than twice as high in the high and average pain sensitivity haplotype groups. This finding may be a result of the combination of single nucleotide polymorphisms into haplotypes because the group typically has stronger associations than individual single nucleotide polymorphisms [75–78]. Correspondingly, haplotype combinations of single nucleotide polymorphisms result in synergistic effects on protein function and, depending on the genes involved (eg, catechol O-methyltransferase), they also

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may be implicated in other disorders, such as comorbid affective conditions. Diatchenko and colleagues [65,79] furthered this line of thought by examining the genetic variations that influence pain amplification and psychological distress. They asserted that the genetic vulnerability coupled with environmental triggers potentially contribute to enhanced pain perception, psychological dysfunction, and the risk of onset of persistent pain conditions, including orofacial pain. As such, the Orofacial Pain Prospective Evaluation and Risk Assessment study, a 7-year multisite research study, is underway to determine predictive factors for the development of chronic orofacial pain (Maixner PI, see NIH website http://crisp.cit.nih. gov/crisp/crisp_lib.query, Grant #5U01Deo171802). The Orofacial Pain Prospective Evaluation and Risk Assessment study will follow individuals for 7 years to determine predictive factors from a range of biopsychosocial and genetic factors. The objective is to lend important evidence to the role of genetics in developing chronic orofacial pain and the moderating and mediating affects of psychological factors and biologic processes. Psychosocial factors In addition to the biologic factors, gender differences in pain perception may be attributed to multiple psychological and social factors. For instance, men and women may differ in their sensitivity to psychological signals, with women exhibiting a greater sensitivity to negative stimuli [15], although Fillingim and colleagues [80,81] and others reported that men experience more anxiety related to pain. Negative affect present in men substantially influences their response to opioids in a negative fashion. Stereotypic gender roles exist in the upbringing of children. For example, young girls are encouraged to report their feelings, yet young boys are discouraged from reporting negative emotions. Such social roles often carry over into how each gender expresses and seeks treatment for pain [82]. Women seek health care services in far greater proportion than men [83]. It has been reported in the literature, and it is typically assumed, that the higher numbers of women seeking care is the result of a greater propensity for pain. There may be neurobiologic reasons, including hormonal influences, for this different proportion of pain reporting, although this is an area of nascent investigation. Historically and even currently, there is a tendency to ascribe this increased pain reporting to psychological or

maladaptive patterns of women. There may be many more reasons for this reporting, however, the complexity and interactions of which are not fully understood. A contributing factor may be social influences that expect women to interface with health care professionals or be more expressive in doing so, whereas men actually may underreport their pain and symptoms. It may be that men and women actually may be experiencing illness in closer ratios than currently reported but the underreporting by men and higher frequency of care-seeking by women may inflate gender disparities [83,84]. Recently, investigators asserted that increased reporting by women may be a result of enhanced sensory discriminability, whereas men may succumb to social roles of demonstrating stoicism rather than reporting actual pain experience [85]. Different occupational roles for men and women may be associated with an increased risk for painful conditions [83,86]. Although stress may not directly cause pain, it has been shown to exacerbate pain and related symptoms. The effects of stress on pain have been reviewed in clinical and nonclinical populations and in nonhuman animal studies [20,87–91]. The mechanisms of action for such responses are complex and involve synergistic interactions and reactions at molecular, biologic, and psychological levels and are the subject of ongoing investigation. Emerging literature suggests that the biologic and physiologic responses to stress are different in men versus women, with multiple endogenous (and exogenous) factorsdmost notably hormonesd influencing variations [22,25,29,92,93]. Because men and women are exposed to different types of stress and respond differently, the experience of pain is likely to be different and presenting symptoms may be characterized differently [94–96]. The definition of stress is important when considering its effects on pain. For example, is one referring to the physiologic reaction to a threat (ie, bodily threat of pain) or other forms of stress, such as anxiety or depression? Psychological processes are well documented as having significant influence on the experience of pain [97–101]. A plethora of literature reports associations of increased pain reports, poor treatment outcome, and increased side effects with negative affect in patient populations [102–106]. In general, women report more frequent and higher levels of pain, more negative affect, and, in some chronic pain conditions, worse outcome [102,107–110]. The literature is replete with studies in clinical settings that have shown the

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influence of depression on pain, and reportedly it is more common in women than men who experience chronic pain [15,22,84,106,111–113], regardless of cause. Importantly, recent neurobiologic and neuroimaging studies of pain and affect have asserted that the chemical and biologic processing of pain and emotion likely run along similar neural pathways, which makes these domains inextricably linked. Although the response to pain and negative affect, such as depression, may have similar corollaries in the neuromatrix, the mechanisms (endogenous and exogenous) and environmental influences of pain and affect processing are postulated to be different between men and women. That finding may help explain the overrepresentation of women in pain reporting negative affect in clinical settings. This trend in gender differences has not been replicated in the experimental realm because men tend to exhibit higher anxiety and, in some cases, greater negative affect. Specifically, the association of anxiety with clinical pain, sensitivity to experimental pain, and treatment-related pain reductions has been shown to be more robust among men than women [29,94,95,114,115]. Investigators [85,96,115] found men to have higher anxiety that was significantly correlated with higher experimental pain. Specifically regarding orofacial pain, researchers have postulated that increased anxiety may predispose individuals to developing various types of chronic orofacial pain and exacerbate underlying diseases [87,116–120]. Recent investigation showed that women reported higher pain intensity and more distress, depression, and inadequate pain relief from medications after dental extraction. Most notable were the associations of distress and depression with higher pain intensity. Likewise, maladaptive pain coping strategies, such as catastrophizing, a common domain assessed in pain research, have been associated with poorer adjustment to clinical pain and higher sensitivity to experimental pain [121–126]. In several instances, investigators have reported higher catastrophizing among women than men [127– 129]. Catastrophizing also has been shown to influence sex differences in the severity of arthritis pain and pain-related disability [128]. Only recently have researchers begun to examine the influence of psychological factors and experimental pain and the effect on analgesic response and side effects. In one of the few studies of its kind to date, Fillingim and colleagues [80] examined experimental pain and analgesic

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response among men and women and discovered that negative affect was negatively associated with analgesic responses for men but not women, whereas negative affect was also more strongly correlated with various pain ratings among men but not women. Catastrophizing was correlated with several analgesic indices among men but not women. In other words, men demonstrated higher catastrophizing scores and less pain relief from opioid medications compared with women. In all cases, higher catastrophizing predicted less robust analgesia. Conversely, positive affect was not associated with analgesic responses, but it was significantly negatively correlated with side effects among men but not women. Catastrophizing was positively correlated with side effects among men but not women such that men with higher catastrophizing scores also displayed significantly more adverse effects from opioids [80,130]. Although these studies did not specifically address orofacial pain, they lend important evidence to understanding multiple factors that influence pain, analgesic response, and mediating factors, such as psychosocial aspects differentially between men and women. Psychological factors are of particular importance to chronic orofacial pain because psychological distress is common among patients who have orofacial pain [12,119,131–136].

Diagnostic criteria for orofacial pain A patient’s history is clearly the most important means of diagnosing chronic orofacial pain and is usually lengthy. Key factors to consider are location of the pain and discerning whether the pain is localized or generalized. The severity and character of the pain should be reported, although many patients who have chronic orofacial pain experience myriad symptoms. Visual analog scales or assessment instruments, such as the McGill Pain Questionnaire, Brief Symptom Inventory, or Multidimensional Pain Inventory, are valuable tools to assess the severity of a patient’s pain and how it impacts their overall daily functions. The average duration of each episode of pain may be helpful in differentiating the cause of the complaint. A ‘‘pain diary’’ is helpful in elucidating a pattern for the occurrence of the pain. For example, pain secondary to temporomandibular joint pain dysfunction may be more severe upon wakening if it is associated with parafunctional habits. Precipitating factors and activities or

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agents that relieve the pain are also important clues for developing a diagnosis. A thorough clinical examination of the head and neck is warranted to eliminate an organic or underlying pathologic cause of the pain. Appropriate imaging studies, such as radiographs, MRI, or CT scans, aid in diagnosis. Because the list of orofacial pain disorders is robust, this article discusses the diagnosis, etiology, and treatment of the more commonly encountered pathologies. For a more detailed list, see Box 1.

Temporomandibular disorders TMDs comprise a broad subgroup of musculoskeletal disorders that affect the temporomandibular joint, the muscles of mastication, and associated structures. TMD has been identified

Box 1. Types of chronic orofacial pain differentiated by etiologic system Neurologic Trigeminal neuralgia Idiopathic trigeminal neuralgia (tic douloureux) Postherpetic neuralgia Vagoglossopharyngeal neuralgia Occipital neuralgia Posttraumatic Multiple sclerosis Sphenopalatine ganglion Burning mouth syndrome Neuropathic Sjo¨gren’s syndrome Diabetic neuropathy Vascular Migraines Tension headaches Cluster headaches Giant cell arteritis Arthogenic Temporomandibular joint disorder Odontogenic Phantom dental pain Atypical odontalgia Myogenic Myofacial pain dysfunction

as one of the most commonly occurring nonodontogenic pain complaints [13]. Recent studies indicate the prevalence of TMD-related pain to be 12% [137]. It is well known that painful TMD is more common in women than men, and women of reproductive age are the demographic group at highest risk for experiencing TMD pain [138,139]. The cause of TMD is complex and multifactorial, and much has been written in the literature relative to experimental and clinical research. Considerable information exists in the literature pertaining to the treatment of TMD, which is based on a conservative or surgical approach and warrants an article in and of itself (the reader is referred to the article on TMD in this issue). Primary headache Primary headache (tension-type and vascular) occurs commonly and is often associated with TMD and disability. Approximately 45 million Americans experience headache pain on a regular basis, which represents a major public health problem [11]. The International Headache Society developed a classification system for headaches in 1988 and categorized tension-type headaches as either episodic or chronic. Episodic tension-type headache is associated with a stressful event and is self-limiting. In general, over-the-counter analgesic medications are successful in relieving the pain. In contrast, chronic tension-type headache is the most common type of recurring head pain and is reported to coexist with TMD in patients. Women have a higher prevalence rate for chronic tension-type headache than men [140]. In the past, the cause of this type of headache was presumed to be muscle contraction of the pericranium; however, no research supports muscular contraction as the sole cause [141]. It is likely that peripheral and central mechanisms are involved. The peripheral trigger, which is thought to begin the process, has not been defined as a single or multiple stimulus acting in an additive process [142]. The International Migraine Society diagnostic criteria for chronic tension-type headache are based on frequency of attacks, associated symptoms, anatomic correlates, and perceived location of pain. A thorough physical examination is essential to eliminate an organic cause of the pain. Treatment varies with the use of nonprescription and prescription analgesics, muscle relaxants, serotonin antagonists, antidepressants,

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nonpharmacologic modalities, acupuncture, and recently, botulinum toxin type A (Botox). Migraine headaches are described as throbbing severe pain that typically occurs on one side of the head and often is accompanied by autonomic nervous system dysfunction and, in some individuals, a transient neurologic symptom described as an aura. The headache may be associated with nausea, vomiting, photophobia, or phonophobia. The pain may last for hours to days. Symptoms may include nasal stuffiness, blurred vision, diarrhea, and abnormal sensations of heat, cold, and irritability. Migraine headaches may begin as early as childhood, have a prevalence of onset between the ages of 35 and 45, and decrease in frequency with age. In fact, an epidemiologic meta-analysis of headaches revealed an unchanging prevalence rate across the life span for men, with approximately 60% experiencing headaches at any given age. In contrast, the prevalence curve for women is relatively flat, with prevalence rates approximately 75% to 80% until approximately age 45, when rates decline. This seems to be the trend for all types of headaches, although the male/female ratio is higher in persons who have migraines [83,86,143]. Approximately 18% of women and 6% of men suffer from migraine headaches, with the disorder affecting approximately 28 million Americans [144]. The cost of lost productivity, medical care, and suffering is profound. The cause of migraine headaches remains unclear, although vascular changes mediated by the release of neuroinflammatory peptides within the brain are thought to be responsible. Many factors have been linked to the development of migraines and include types of food, stress, activity, and gonadal hormones. It is known that migraine headaches are associated with the natural changes in levels of ovarian steroids during the menstrual cycle and at menopause [145,146]. The drop of estrogen before menstruation elicits menstrual migraines, which may be more severe than other types of migraine headaches. Likewise, migraine headaches diminish during pregnancy, when estrogen levels are elevated, and after menopause, when fluctuating estrogen levels abate. A recent study revealed an alarming association of migraines with other life-threatening diseases. The investigation of a large prospective cohort of women with active migraine headaches with aura indicated that they were at increased risk for major cardiovascular disease, myocardial infarction, and ischemic stroke compared with

patients with migraines without aura [147]. These recent findings underscore the importance of treating migraines aggressively and effectively. Treatment of migraine headaches includes acute medication such as triptans, ergots, and analgesics or prophylactic treatments such as b-blockers, calcium-channel blockers, serotonin antagonists, antidepressants, and antiepileptic drugs and nonpharmacologic therapies such as relaxation therapy, biofeedback, stress management, B vitamin supplements, elimination diet, and acupuncture. As with tension-type headaches, treatment with botulinum toxin type A is receiving considerable attention. Botulinum toxin type A (Botox) is a neurotoxin produced by the anaerobic bacterium, Clostridium botulinum. Botulinum toxin has been approved by the US Food and Drug Administration for therapeutic use for involuntary human muscle hyperactivity, blepharospasm and strabismus, cervical dystonia, severe primary axillary hyperhidrosis, and cosmetic use for glabellar rhytides. Table 1 lists the US Food and Drug Administration approvals for use of Botox. Off-label use of botulinum toxin has been reported in the treatment of many orofacial conditions, including primary headaches, migraine headaches, masticatory and facial muscle spasm, idiopathic hypertrophy of the masticatory muscles, myofascial pain, chronic neuropathic pain, and episodic trigeminal neuralgia (TN). Botulinum toxin acts by interfering with vesicular exocytosis at synaptic junctions and inhibits the release of the neurotransmitters contained within the vesicles, primarily acetylcholine [148]. In vitro and in vivo evidence suggests that botulinum toxin also inhibits the release of nociceptive mediators, such as glutamate, substance P, and calcitonin gene-related peptide from nociceptive fibers in a peripheral mechanism [149–151]. The data reported in the literature on the use of botulinum toxin A for off-label use are preliminary, much of which are case reports or clinical trials with contradictory results. Evidence Table 1 On-label, US Food and Drug Administration–approved uses of botulinum toxin type A Condition

Date of approval

Cervical dystonia Glabellar lines Axillary hyperhydrosis

December, 21, 2000 April 12, 2002 July 19, 2004

Data from http://www.accessdata.fda.gov/.

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emerging from randomized, double-blind, and placebo-controlled studies suggests that the use of botulinum toxin A may have optimistic results for the prophylactic treatment of migraine headaches [152,153].

Trigeminal neuralgia TN is a well-recognized disorder of the orofacial region characterized by lancinating, unilateral, paroxysmal pain that occurs along the distribution of the fifth cranial nerve. The rate of occurrence of TN in women and men is 5.7 and 2.5 per 100,000 per year, respectively [154]. The diagnosis is based primarily on the history of characteristic pain criteria, which has received considerable attention in research and clinical studies. These criteria emphasize five major clinical features, as described by White and Sweet [155]: (1) paroxysmal pain, (2) pain provoked by light touch to trigger zones, (3) pain confined to trigeminal distribution, (4) unilateral pain, and (5) normal clinical neurosensory examination. Patients with a diagnosis of TN are symptom free between attacks. In most patients with TN, their clinical examination, imaging studies, and laboratory test results are normal (‘‘classic TN’’) as opposed to a smaller group of patients with TN whose symptoms are secondary to another disease process that affects the trigeminal system [156]. The pathophysiology of TN is unclear. Injury to the trigeminal nerve root by a benign tumor or vascular anomaly has been found to produce symptoms clinically indistinguishable from classic TN [157]. Focal demyelination at the site of compression may elicit the characteristic sudden ‘‘electric’’ insults that characterize TN [156]. The treatment modalities for the management of TN may be divided into medical, surgical, or gamma-knife radiosurgery. The use of antiepileptic drugs has gained considerable success, such as gabapentin, baclofen, or clonazepam. Antidepressants, opioids, and topical agents also have been used, but efficacy has not been supported by well-controlled clinical trials [158]. The use of botulinum toxin injections has been reported in the literature with positive results, although few patients have been treated in this way and none in a controlled setting [159–161]. Surgical techniques include percutaneous radiofrequency trigeminal gangliolysis, percutaneous balloon microcompression, microvascular decompression, endoscopic

vascular decompression, and retrogasserian rhizotomy [156,162,163]. Persistent idiopathic facial pain Chronic facial pain is a constant chronic orofacial discomfort or pain defined by the International Headache Society as facial pain not fulfilling other criteria [162]. Several terms have been used to describe this disorder, including the commonly used terms ‘‘atypical facial pain’’ or ‘‘chronic facial pain.’’ The International Headache Society [164] has coded this entity as ‘‘persistent idiopathic facial pain’’, however (code 13.18.4). Patients often experience a dull or burning type of pain in an ill-defined area. The distribution of the pain is not related to the anatomic distribution of the trigeminal nerve. The paindintraoral or extraoraldmay persist for much of the day but rarely wakes an individual at night, although patients may report difficulty in sleeping. It has been reported that an association exists between patients with persistent idiopathic facial pain and other medical disorders or general pain conditions [165,166]. The incidence of persistent idiopathic facial pain is greater in women than men [15,17,18,22]. The diagnosis of persistent idiopathic facial pain is a difficult one to make because these patients commonly have multiple complaints and frequently have undergone multiple surgical procedures without success to alleviate their pain. The referred pattern of facial pain contributes to the demanding nature of diagnosing persistent idiopathic facial pain. An unremarkable clinical examination, negative imaging studies, and hematologic evaluation lead one to the diagnosis. Antidepressants have been used successfully in the treatment of persistent idiopathic facial pain. Anticonvulsants, such as gabapentin (Neurontin) and pregabalin (Linsea), have been used with success, and clinical trials have revealed decreased pain, increased function, and improved quality of life among patients with such treatment [158,167–175]. Serotonin selective reuptake inhibitors have not earned a consistently successful reputation for use in the treatment of atypical facial pain [176]. Managing orofacial pain The goal in managing patients with chronic orofacial pain is to reduce or eliminate their pain, correct the disease process if possible, and aid in

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improving their quality of life. Clearly, in the last decade, much research has focused on elucidating gender differences in the response to pain. An accurate diagnosis, although often elusive and laborious to achieve, is essential in the treatment of orofacial pain. A multidisciplinary team approach is recommended to include a medical and dental practitioner, psychologist, physical therapist, and pain management specialist. In the past two decades, the importance of the multidisciplinary team has been validated in multiple clinical settings, and such research is growing in the area of orofacial pain. Multiple investigations have reported the beneficial diagnostic and treatment outcomes that lead to long-term functional restoration, improved pain management, enhanced coping, and overall mood improvement. Given the complexity of orofacial pain, it is imperative to seek to incorporate a multidisciplinary approach. This approach has the potential only to augment clinical efficacy but also to ultimately improve the quality of life for patients who suffer from these disorders. Clearly, the advances in clinical pain research may help guide us to advantageous treatment modalities for a given patient and achieve an improved quality of life. References [1] Merskey H, Bogduk N. Classification of chronic pain. Seattle (WA): IASP Press; 1994, 45–47. [2] Sternbach RA. Survey of pain in the United States: the Nuprin pain report. Clin J Pain 1986;2:49–53. [3] Sternbach RA. Pain and hassles in the United States: findings of the Nuprin pain report. Pain 1986; 27(1):69–80. [4] Baker TA, Whitfield KE. Physical functioning in older blacks: an exploratory study identifying psychosocial and clinical predictors. J Natl Med Assoc 2006;98(7):1114–20. [5] Karoly P, Ruehlman LS, Aiken LS, et al. Evaluating chronic pain impact among patients in primary care: further validation of a brief assessment instrument. Pain Med 2006;7(4):289–98. [6] Portenoy RK, Ugarte C, Fuller I, et al. Populationbased survey of pain in the United States: differences among white, African American, and Hispanic subjects. J Pain 2004;5(6):317–28. [7] Nicholson RA, Rooney M, Vo K, et al. Migraine care among different ethnicities: do disparities exist? Headache 2006;46(5):754–65. [8] Agostoni E, Frigerio R, Santoro P. Atypical facial pain: clinical considerations and differential diagnosis. Neurol Sci 2005;26(Suppl 2):s71–4. [9] Madland G, Newton-John T, Feinmann C. Chronic idiopathic orofacial pain: I. What is the evidence base? Br Dent J 2001;191(1):22–4.

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