Chapter 8 NONODONTOGENIC TOOTHACHE AND CHRONIC HEAD AND NECK PAINS

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1 Chapter 8 NONODONTOGENIC TOOTHACHE AND CHRONIC HEAD AND NECK PAINS Bernadette Jaeger Pain is perfect misery, the worst of evils; and excessive, overturns all patience. John Milton, Paradise Lost Patients with chronic oral or facial pain, or headache, present a true diagnostic and therapeutic challenge to the practitioner. For many in the dental profession, the only solution to problems of pain lies with a scalpel, forceps, or ever-increasing doses of analgesics, narcotics, or sedatives. Many patients with chronic pain have suffered this mistreatment and stand as an indictment of a poorly trained, insecure, and disinterested segment of dentistry. Attending to patients who have been unable to obtain resolution of their pain complaint, despite extensive evaluation and treatment, requires a compassionate reappraisal and fresh approach. Fortunately, accurate diagnosis and successful management of these patients can be among the most rewarding experiences in dental or medical practice. WHAT IS PAIN? Pain is not a simple sensation but rather a complex neurobehavioral event involving at least two components. First is an individual s discernment or perception of the stimulation of specialized nerve endings designed to transmit information concerning potential or actual tissue damage (nociception). Second is the individual s reaction to this perceived sensation (pain behavior). This is any behavior, physical or emotional, that follows pain perception. Culture or environment often influences these behaviors. Beyond this is the suffering or emotional toll the pain has on any given individual. Suffering is so personal that it is difficult to quantify, evaluate, and treat. The fact that pain is difficult to define, quantify, and understand is reflected in the numerous ways in which it has been described. Dorland s Medical Dictionary defines pain as a more or less localized sensation of discomfort, distress, or agony resulting from the stimulation of specialized nerve endings. 1 In this definition, the behavioral reaction to nociception is already assumed to be distress or agony, which is not always the case. Take, for example, the observations made by Beecher in 1956 that only 25% of soldiers wounded in battle requested narcotic medications for pain relief, compared to more than 80% of civilian patients with surgical wounds of a similar magnitude. 2 Clearly, the behavioral reaction to similar nociceptive stimuli varies from person to person and depends on a number of factors, including the significance of the injury to that individual. The wounded soldier may be relieved to be out of a life-threatening situation; the surgical patient may be concerned about recurrence of a tumor just removed. Dorland s definition also implies that stimulation of nociceptors is required for perception of pain, yet the dental patient who has been anxious for weeks in anticipation of the needle at the dentist s office may jump in agony at the slightest touch of his cheek. Fields defined pain as an unpleasant sensation that is perceived as arising from a specific region of the body and is commonly produced by processes that damage or are capable of damaging bodily tissue. 3 He emphasized the need to be able to localize the painful source in order to distinguish it from psychological pain and suffering, for example, the pain of a broken heart. A more complete definition is cast by the International Association for the Study of Pain (IASP) in its taxonomy of painful disorders. 4 That definition of pain is as follows: An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. Added to this definition, however, is the following, emphasizing the subjective nature of pain that distinguishes and separates it from the simple stimulation of nociceptors:

2 288 Endodontics Pain is always subjective. Each individual learns the application of the word through experiences related to injury in early life. It is unquestionably a sensation in a part of the body, but it is also always unpleasant and therefore also an emotional experience. Many people report pain in the absence of tissue damage or any likely pathophysiological cause, usually this happens for psychological reasons. There is no way to distinguish their experience from that due to tissue damage, if we take the subjective report. If they regard their experience as pain and if they report it in the same ways as pain caused by tissue damage, it should be accepted as pain. This definition avoids tying pain to the stimulus. Activity induced in the nociceptor and nociceptive pathways by a noxious stimulus is not pain, which is always a psychological state, even though we may well appreciate that pain most often has a proximate physical cause. 4 The IASP definition of pain makes the point that pain is pain even if a nociceptive source is not readily identified. Pain owing to psychological causes is as real as any pain associated with actual nociception and should be treated as such. To understand pain better, this chapter first looks at what is currently known about the anatomy and physiology of the nociceptive pathways and some of the modulating influences that modify the nociceptive input into the central nervous system. Following this, various psychological and behavioral factors that influence the perception of and reaction to pain are reviewed. NEUROPHYSIOLOGY OF PAIN The following summarizes what is known about the basic anatomy and physiology of pain under normal physiologic conditions 5 : Acute Pain Pathways The body has specialized neurons that respond only to noxious or potentially noxious stimulation. These neurons are called primary afferent nociceptors and are made up of small-diameter thinly myelinated A delta and unmyelinated C fibers (Figure 8-1). They synapse in the substantia gelatinosa of the dorsal horn of the spinal cord with neurons known as second-order pain transmission neurons. From here the signals are transmitted along specialized pathways (spinothalamic and reticulothalamic tracts) to the medial and lateral A Figure 8-1 Components of a typical cutaneous nerve. A illustrates that there are two distinct functional categories of axon: primary afferents with cell bodies in the dorsal root ganglion and sympathetic postganglionic fibers with cell bodies in the sympathetic ganglion. Primary afferents include those with large-diameter myelinated (Aα), smalldiameter myelinated (Ad), and unmyelinated (C) axons. All sympathetic postganglionic fibers are unmyelinated. B, Electron micrograph of cross-section of a cutaneous nerve illustrating the relative size and degree of myelination of its complement of axons. The myelin appears as black rings of varying thickness. The unmyelinated axons (C) occur singly or in clusters. Reproduced with permission from Ochoa JL. Microscopic anatomy of unmyelinated nerve fibers. In: Dyck PJ, et al, editors. Peripheral neuropathy. 1st ed. WB Saunders; Philadelphia (PA): B

3 Nonodontogenic Toothache and Chronic Head and Neck Pains 289 regions of the thalamus (Figure 8-2). Perception of nociception may occur in the thalamus and cortex, but the exact location is unknown, and the contribution of the cortex to pain perception is controversial. 3 Fields divided the processing of pain from the stimulation of primary afferent nociceptors to the subjective experience of pain into four steps: transduction, transmission, modulation, and perception. 3 Transduction is the activation of the primary afferent nociceptor. Primary afferent nociceptors can be activated by intense thermal and mechanical stimuli, noxious chemicals, and noxious cold. They are also activated by stimulation from endogenous algesic chemical substances (inflammatory mediators) produced by the body in response to tissue injury. Damaged tissue or blood cells release the polypeptide bradykinin (BK), potassium, histamine, serotonin, and arachidonic acid. Arachidonic acid is processed by two different enzyme systems to produce prostaglandins and leukotrienes, which, along with BK, act as inflammatory mediators (Figure 8-3). Bradykinin acts synergistically with these other chemicals to increase plasma extravasation and produce edema. Plasma extravasation, in turn, replenishes the supply of inflammatory chemical mediators. Whereas prostaglandins stimulate the primary afferent nociceptor directly, the leukotrienes contribute indirectly by causing polymorphonuclear neutrophil leukocytes to release another chemical, which, in turn, stimulates the nociceptor. Bradykinin further contributes by causing the sympathetic nerve terminal to release a prostaglandin that also stimulates the nociceptor. 6 Additionally, in an area of injury or inflammation, the sympathetic nerve terminal will release yet another prostaglandin in response to its own neurotransmitter, norepinephrine. The presence of such an ongoing inflammatory state causes physiologic sensitization of the primary afferent nociceptors. 6 Sensitized nociceptors display ongoing discharge, a lowered activation threshold to normally nonpainful stimuli (allodynia), and an exaggerated response to noxious stimuli (primary hyperalgesia). 7 In addition to sending nociceptive impulses to synapse in the dorsal horn of the spinal cord, activation of cutaneous C fibers causes their cell bodies to synthesize the neuropeptides, substance P and calcitonin gene related peptide (CGRP). These neuropeptides are then antidromically transported along axon branches to the periphery by an axon transport system where they induce further plasma extravasation and increase inflammation. The release of these algogenic substances at the peripheral axon injury site produces the flare commonly seen around an injury site and is referred to as neurogenic inflammation or the axon reflex 7 9 (Figure 8-4). Transmission refers to the process by which peripheral nociceptive information is relayed to the central Figure 8-2 Diagrammatic outline of major neural structures relevant to pain. Sequence of events leading to pain perception begins in the transmission system with transduction (lower left), in which a noxious stimulus produces nerve impulses in the primary afferent nociceptor. These impulses are conducted to the spinal cord, where primary afferent nociceptors contact central pain transmission cells, which relay the message to the thalamus either directly via the spinothalamic tract or indirectly via the reticular formation and the reticulothalamic pathway. From the thalamus, the message is relayed to the cerebral cortex and the hypothalamus (H). The outflow is through the midbrain and medulla to the dorsal horn of the spinal cord, where it inhibits pain transmission cells, thereby reducing the intensity of perceived pain. Reproduced with permission from Pain and disability, copyright 1987 by the National Academy of Sciences. Published by National Academy Press, Washington, DC.

4 290 Endodontics Figure 8-3 Membrane lipids produce arachidonic acid, which is converted to prostaglandins by the cyclooxygenase enzyme and to leukotriene B 4 by the lipoxygenase enzyme. Prostaglandins act directly on the primary afferent nociceptor to lower the firing threshold and therefore cause sensitization. Leukotriene B 4 cause polymorphonuclear neutrophil leukocytes (PMNLs) to produce another leukotriene that, in turn, acts on the primary afferent nociceptor to cause sensitization. Steroids prevent the synthesis of arachidonic acid altogether, thus inhibiting both pathways of prostaglandin production. Nonsteroidal anti-inflammatory drugs (NSAIDs), on the other hand, inhibit only the cyclooxygenase pathway. Figure 8-4 The axon reflex. Activation of cutaneous nociceptive C fibers elicits impulses that are conveyed centrally to induce pain and antidromically via axon branches (A). The antidromically excited peripheral C-fiber terminals release vasoactive substances, for example, calcitonin gene related peptide (CGRP) and substance P (SP), causing cutaneous vasodilation, which produces the flare that develops around the site of noxious stimulation. Reproduced with permission from Fields HL, Rowbotham M, Baron R. Neuralgia: irritable nociceptors and deafferentation. Neurobiol Dis 1998;5:209. nervous system. The primary afferent nociceptor synapses with a second-order pain transmission neuron in the dorsal horn of the spinal cord where a new action potential heads toward higher brain structures (see Figure 8-2). It is at this point that repeated or intense C fiber activation causes specific changes involving substance P and excitatory amino acids acting on N-methyl-D-aspartate (NMDA) receptors that results in central sensitization. 7 Long-term changes in the response of second-order pain transmission neurons to nonpainful and painful input are induced with intense or prolonged nociceptive stimuli. 7 The response of these spinal cord dorsal horn neurons increases progressively and is enhanced with repeated identical noxious cutaneous input from the periphery, a process called wind-up In addition, the size of the receptive field of the second-order pain transmission neuron increases. 13 The subjective correlate of wind-up is temporal summation, for which a slowly repeated noxious stimulus is associated with a progressive increase in the intensity of perceived pain. 7,14 In addition, with central sensitization, stimulation of A beta fibers (large-diameter low-threshold mechanoreceptors that normally respond only to painless tactile

5 Nonodontogenic Toothache and Chronic Head and Neck Pains 291 stimuli) will also activate second-order nociceptive dorsal horn neurons, producing what is called a secondary mechanical hyperalgesia in the area surrounding the initial tissue injury 7,15 (Figure 8-5). Modulation refers to mechanisms by which the transmission of noxious information to the brain is reduced. Numerous descending inhibitory systems that originate supraspinally and strongly influence spinal nociceptive transmission exist. 16 In the past, only midline structures such as the periaqueductal gray and nucleus raphe magnus were known to be involved in descending nociceptive modulation (Figure 8-2). Now many sites previously thought to be primarily involved in cardiovascular function and autonomic regulation (eg, nucleus tractus solitarius; locus ceruleus/subceruleus, among others) have also been shown to play a role in pain modulation. 16 The ascending nociceptive signal that synapses in the midbrain area activates the release of norepinephrine (NE) and serotonin, two of the main neurotransmitters involved in the descending inhibitory pathways. 16 Activity in the pain modulation system means that there is less activity in the pain transmission pathway in response to noxious stimulation. Figure 8-5 Central sensitization and allodynia. Input from C- nociceptors enhances the response of dorsal horn pain-signaling neurons to subsequent afferent inputs (central sensitization). This involves neuropeptides such as substance P (SP) acting at neurokinin receptors (NKR) and excitatory amino acids (EAA) acting at both the AMPA/KA and N-methyl-D-aspartate (NMDA) receptors, triggering secondary NO (nitric oxide) mechanisms. Largediameter low-threshold mechanoreceptive primary afferents (A beta fibers) respond maximally to innocuous tactile stimuli and normally produce tactile sensation. When central sensitization is present, A beta fibers become capable of activating central nervous system pain-signaling neurons (+), leading to touch-evoked pain (allodynia). Reproduced with permission from Fields HL, Rowbotham M, Baron R. Neuralgia: irritable nociceptors and deafferentation. Neurobiol Dis 1998;5:209. An endogenous opioid system for pain modulation also exists. 17 Endogenous opioid peptides are naturally occurring pain-dampening neurotransmitters and neuromodulators that are implicated in pain suppression and modulation because they are present in large quantities in the areas of the brain associated with these activities (subnucleus caudalis and the substantia gelatinosa of the spinal cord). 17,18 They reduce nociceptive transmission by preventing the release of the excitatory neurotransmitter substance P from the primary afferent nerve terminal. The presence of these natural opioid receptors for endogenous opiates permits morphine-like drugs to exert their analgesic effect. The final step in the subjective experience of pain is perception. How and where the brain perceives pain is still under investigation. Part of the difficulty lies in the fact that the pain experience has at least two components: the sensory-discriminatory dimension and the affective (emotional) dimension. The affective dimension of pain is made up of feelings of unpleasantness and emotions associated with future implications related to the pain. 19 Although functional magnetic resonance imaging (MRI) studies have demonstrated the involvement of the thalamus and multiple cortical areas in the perception of pain, it is clear from the intersubject variability in the activation of any one of these areas that affective reactions and possibly motor responses are also involved. 20 Of significance is the fact that, with high levels of modulation, or with damage in the pain transmission system, it is possible to have nociception without pain perception. Conversely, with certain types of damage to the nervous system, there may be an overreaction to pain stimuli or pain perception without nociception. 3 Referred Pain Pain arising from deep tissues, muscles, ligaments, joints, and viscera is often perceived at a site distant from the actual nociceptive source. Thus, the pain of angina pectoris is often felt in the left arm or the jaw, and diaphragmatic pain is often perceived in the shoulder or neck. Whereas cutaneous pain is sharp, burning, and clearly localized, referred pain from musculoskeletal and visceral sources is usually deep, dull, aching, and more diffuse. Referred pain presents a diagnostic dilemma. If left unrecognized, it may result in a clinician telling a patient that his pain is psychogenic in origin. Treatments directed at the site of the pain are ineffective and, if invasive, subject the patient to unnecessary risks, expense, and complications. However, referred pain is dependent on a primary pain source and will cease if this source is eliminated.

6 292 Endodontics The mechanism of referred pain is still somewhat enigmatic. The two most popular theories are convergence-projection and convergence-facilitation: 1. Convergence-projection theory: This is the most popular theory. Primary afferent nociceptors from both visceral and cutaneous neurons often converge onto the same second-order pain transmission neuron in the spinal cord, 21 and convergence has been well documented in the trigeminal brainstem nuclear complex The trigeminal spinal tract nucleus also receives converging input from cranial nerves VII, IX, and X, as well as the upper cervical nerves. 26,27 The brain, having more awareness of cutaneous than of visceral structures through past experience, interprets the pain as coming from the regions subserved by the cutaneous afferent fibers (Figure 8-6). 2. Convergence-facilitation theory: This theory is similar to the convergence-projection theory, except that the nociceptive input from the deeper structures causes the resting activity of the second-order pain transmission neuron in the spinal cord to increase or be facilitated. The resting activity is normally created by impulses from the cutaneous afferents. Facilitation from the deeper nociceptive impulses causes the pain to be perceived in the area that creates the normal, resting background activity. This theory tries to incorporate the clinical observation that blocking sensory input from the reference area, with either local anesthetic or cold, can sometimes reduce the perceived pain. This is particularly true with referred pain from myofascial trigger Figure 8-6 The convergence-projection hypothesis of referred pain. According to this hypothesis, visceral afferent nociceptors (S) converge on the same pain-projection neurons as the afferents from the somatic structures in which the pain is perceived. The brain has no way of knowing the actual source and mistakenly projects the sensation to the somatic structure. Reproduced with permission from Fields HL. 3 points (TrPs), for which application of a vapocoolant spray is actually a popular and effective modality used for pain control. The mechanism of referred pain from myofascial TrPs is also under speculation. According to Mense, the convergence-projection and convergence-facilitation models of referred pain do not directly apply to muscle pain because there is little convergence of neurons from deep tissues in the dorsal horn. 28 Based on experimentally induced changes in the receptive field properties of dorsal horn neurons in the cat in response to a deep noxious stimulus 29 (Figure 8-7), Mense proposed that convergent connections from other spinal cord segments are unmasked or opened by nociceptive input from skeletal muscle and that referral to other myotomes is owing to the release and spread of substance P and CGRP to adjacent spinal segments 28 (Figure 8-8). Simons has expanded on this theory to specifically explain the referred pain from TrPs 30 (Figure 8-9). Myofascial pain (MFP) is discussed in more detail later in the chapter. Trigeminal System An appreciation of the arrangement of the trigeminal nociceptive system provides some insight into the interesting pain and referral patterns that are encountered in the head and neck region. The primary afferent nociceptors of the fifth cranial nerve synapse in the nucleus caudalis of the brainstem. The nucleus caudalis is the caudal portion of the trigeminal spinal tract nucleus and corresponds to the substantia gelatinosa of the rest of the spinal dorsal horn (Figure 8-10). From here the nociceptive input is transmitted to the higher centers via the trigeminal lemniscus. Of significance is the arrangement of the trigeminal nerve fibers within this nucleus and the fact that the nucleus descends as low as the third and fourth cervical vertebrae (C3 4) in the spinal cord. Fibers from all three trigeminal branches are found at all levels of the nucleus, arranged with the mandibular division highest and the ophthalmic division lowest. 31 In addition, they are arranged in such a manner that fibers closest to the midline of the face synapse in the most cephalad portion of the tract. The more lateral the origin of the fibers on the face, the more caudal the synapse in the nucleus (Figure 8-11). Understanding this laminated arrangement helps to explain why a maxillary molar toothache may be perceived as pain in a mandibular molar on the same side (referred pain) but not in an incisor. Similarly, pain perceived in the ear may actually be owing to (or referred from) an infected third molar.

7 Nonodontogenic Toothache and Chronic Head and Neck Pains 293 Figure 8-7 Changes in receptive field (RF) properties of a dorsal horn neuron following intramuscular injection of a painful dose of bradykinin (BKN). A, Location and size of the original RF (black) before BKN injection. The neuron required noxious deep pressure stimulation (Nox. p. deep) of the proximal biceps femoris muscle for activation. The arrow points to the injection site in the anterior tibial muscle (TA). B, left, 5 minutes after the BKN injection, two new RFs were present (black), both of which were located in deep tissues and had a high mechanical threshold. B, right, 15 minutes after the BKN injection, the original RF displayed a lowering in mechanical threshold and now responded to moderate (innocuous) deep pressure (Mod. p. deep). Reproduced with permission from Mense S. 28 Figure 8-8 Neuroanatomic model explaining the appearance of new receptive fields (RFs) (see Figure 8-7) by unmasking latent connections in the dorsal horn. The activity of neuron 1 was recorded with a microelectrode introduced into the spinal cord. The neuron is connected by pathway A to its original RF in the biceps femoris muscle (RF I). Synaptically effective connections are drawn as solid lines, ineffective (latent) connections as dashed lines. The injection of bradykinin was made outside RF I into the tibialis anterior (TA) muscle, which contains the RF of neuron 2 (RF II). The bradykinin-induced excitation of nociceptive fibers of pathway B is assumed to release substance P (SP) and calcitonin gene related peptide (CGRP) in the dorsal horn, which diffuse (stippling) to neuron 1 and increase the efficacy of latent connections from pathways B and C to this cell. Now neuron 1 can be activated also from RF II and RF III. (Menses, unpublished data). Reproduced with permission from Mense S. 28 Figure 8-9 Extension of the neuroanatomic model presented in Figure 8-7 of Mense s model of deep referred pain. Although no direct experimental evidence substantiates this modification, it is compatible with the mechanisms described by Mense and helps to explain some trigger point characteristics not accounted for by his model. Neurons 1 and 2 correspond to neurons 1 and 2 in the Mense model. Neurons 1 and 4 are connected by solid lines to their respective receptive fields. These fields are the areas that would be identified as the source of nociception when neurons 1 and 4 are activated. Nociceptive input from the trigger point would activate neuron 2 and could account for the initial localized pain in response to pressure applied to the trigger point. This activity is assumed to release substance P (SP) and calcitonin gene related peptide (CGRP) in the dorsal horn that diffuses (stippling) to neurons 1 and 4. This increases the efficacy of latent connections (dashed lines) to these cells. Now neurons 1 and 4 can be activated by nociceptive activity originating in the trigger point and would be perceived as referred pain. Reproduced with permission from Simons DG. 30

8 294 Endodontics Figure 8-10 Primary afferent nociceptive fibers of the trigeminal nerve (cranial nerve V) synapse in the nucleus caudalis of the spinal trigeminal tract. The nucleus caudalis descends as low as C3 4 in the spinal cord. Many nociceptors from deep cervical structures synapse on the same second-order pain transmission neurons as the trigeminal nerve. This may explain why cervical pain disorders are often perceived as facial pain or headache. Because the trigeminal nucleus descends to the C3 4 level in the spinal cord, primary afferent nociceptors from deep cervical structures synapse on the same second-order pain transmission neurons that subserve the fifth cranial nerve. 32 This convergence of primary afferent nociceptors from the trigeminal region and the cervical region provides a basis for understanding why cervical pain disorders may be perceived as pain in the head and face, particularly in the forehead and temple the lateral ophthalmic trigeminal fibers synapse the lowest (see Figure 8-11). Chronic Pain Pain becomes complicated and difficult to manage when it is prolonged. Often the clinician is frustrated by the apparent discrepancy between the identifiable nociceptive source, which may seem very small, and the amount of suffering and disability seen. It becomes easy to label these patients as crazy or malingering (deliberately, fraudulently feigning an illness for the purpose of a consciously desired outcome). 1 Yet there are both physiologic and psychological mechanisms that may increase pain perception mechanisms that help to explain why there may be a discrepancy between actual nociception, perceived pain, and the apparent resultant suffering and disability. Physiologic Mechanisms Modifying Pain. Sensitization. As previously discussed, primary afferent nociceptors become sensitized through the release of endogenous substances caused by tissue injury. As a

9 Nonodontogenic Toothache and Chronic Head and Neck Pains 295 Figure 8-12 Reflex activation of nociceptors in self-sustaining pain. There are two important reflex pathways for pain. The top loop illustrates the sympathetic component. Nociceptor input activates sympathetic reflexes, which activate or sensitize nociceptor terminals. The bottom loop illustrates the muscle contraction loop. Nociceptors induce muscle contraction, which, in some patients, activates muscle nociceptors that feed back into the same reflex to sustain muscle contraction and pain. Reproduced with permission from Pain and disability, copyright 1987 by National Academy of Sciences. Published by National Academy Press, Washington, DC. Figure 8-11 The arrangement of the trigeminal nociceptive fibers of the spinal trigeminal tract is significant. Fibers from all three trigeminal branches are found at all levels of the nucleus, arranged with the mandibular division highest and the ophthalmic division lowest. Fibers closest to the midline of the face synapse in the most cephalad portion of the tract. The more lateral the origin of the fibers on the face, the more caudal the synapse in the nucleus. Reproduced with permission from Kunc Z. 31 result, normally innocuous stimuli become painful. 6 For example, acute arthritis of the temporomandibular joint (TMJ) results in pain on joint movement or with increased pressure from chewing, normally innocuous events. Similarly, a minor burn on the tongue from hot tea makes it almost impossible to eat anything even mildly spicy. Spreading Muscle Spasm. Sustained muscle contraction (spasm) may arise as the result of a primary noxious stimulus. This is a spinal reflex and a protective response to tissue injury (Figure 8-12). An example of this would be masticatory elevator muscle spasm (trismus) secondary to an infected third molar. The spasm may actually be the chief complaint, and yet, initially, it is dependent on the primary pain source. However, if the muscle spasm results in ischemia and accumulation of potassium ions, muscle nociceptors may be activated, resulting in the development of an independent, self-perpetuating primary pain source in the muscle (see Figure 8-12). Successful treatment of the infection or removal of the painful third molar will no longer correct the muscle pain problem since use of the muscle produces pain, causing more spasm, causing more pain. In addition, studies have shown that this type of deep musculoskeletal pain causes spasm and pain in other muscles innervated by the same spinal segment. 33,34 Long-standing conditions of this sort may result in recruitment of more muscles and more pain, with the ultimate establishment of a vicious spreading pain cycle. This may partly explain the development and some of the characteristics of myofascial TrPs, to be discussed in detail later in the chapter. Autonomic Factors. Just as primary afferent nociceptive input may activate motoneurons, so may it also activate the sympathetic nervous system (see Figure 8-12). Efferent discharge from the sympathetic nervous system has been shown, in animals at least, to activate primary afferent nociceptors, especially when

10 296 Endodontics injured. 35 Thus, a peripheral injury may set up a positive feedback loop through activation of the sympathetic nervous system that will perpetuate the activation of the primary afferent nociceptors. The extreme result of this type of sympathetic hyperactivity is a condition known as reflex sympathetic dystrophy (discussed in more detail later in this chapter). In this syndrome, the pain, even from a minor injury, does not subside and, in fact, develops into a progressive, excruciating burning pain with cutaneous hypersensitivity. The pain may occur in a site larger than and different from that of the original injury; autonomic signs such as vasoconstriction or sweating of the painful area are usually present. The sympathetic nervous system is strongly implicated because sympathetic blockade abolishes the pain. Mild forms of this self-perpetuating loop of sympathetic activity and primary nociceptive response may explain why pain sometimes worsens, even when the injury has healed. Psychological Factors Modifying Pain. Three thresholds for sensation and pain help in understanding the subjective experience of pain. Sensory threshold, pain threshold, and pain tolerance (or response threshold ) refer to the specific levels in the sensory continuum where intensity of stimulation meets a change in conscious experience. Joy and Barber used an example of a human subject, stimulated with an increasing-intensity electrical current to the finger, to help distinguish each of the thresholds. 36 The first time the subject reports perception of any sensation is termed the sensory threshold. This is defined as the lowest level of stimuli that will cause any sensation the summation of large sensory fibers from receptors for touch, temperature, and vibration. As the current is increased, the sensation becomes stronger until the subject states that it is painful. This is the pain threshold and has been shown to be fairly constant among individuals. 15,37 Neurologically, when the summation of firing of primary afferent nociceptive fibers reaches a certain point, pain is perceived. If the intensity of the electrical current is increased above pain threshold, a level of pain will be reached that the subject can no longer endure. This is pain tolerance or the response threshold. At this point, the individual makes an attempt to withdraw from the stimulus. The range between the pain threshold and response threshold is termed a person s tolerance to pain, that is, the amount of pain that can be tolerated after pain is first perceived. Although the pain threshold is relatively constant among different people, pain tolerance varies greatly. This is because perception of sensations and tolerance to pain vary in relation to many cognitive, affective (emotional) factors. Cognitive and Affective Factors. Sensory factors include the detection, localization, quantification, and identification of the quality of a particular stimulus. Reaction to the stimulus, the intensity of desire to terminate the stimulus, is determined by cognitive and affective variables. Cognitive variables include such things as an individual s past experience with similar stimuli, their psychological makeup, and societal and cultural factors. Affective variables relate to emotions and feelings and determine how unpleasant the stimulus is to the individual. Affective descriptors of a sensory experience might include words such as nagging, uncomfortable, intense, or killing, in contrast to sensory features such as mild burning, localized to the palate, or aching over the TMJ. Affective variables may be accompanied by anxiety or depression and are influenced by expectation and suggestion. For example, most people are not particularly distressed about having a headache since the vast majority of headaches are not pathologic. Yet someone whose sibling recently died of a brain tumor might be much more worried and anxious about this same symptom, even if it is very mild. Similarly, recurrence of pain owing to cancer carries with it the knowledge that the disease may be progressing and may remind the individual of his mortality. This type of pain will have many more emotional components and may be perceived as much more severe. Another good example is the anxious dental patient who jumps in agony at the first touch of the cheek. Even though the sensation of touch is well below his experimental pain threshold, the patient perceives it and reacts to it as painful. Conversely, a person experiencing analgesia through hypnosis may perceive no sensations or only nonpainful sensations while undergoing normally painful procedures such as tooth extraction or pulp extirpation. 38,39 Frontal lobotomy reduces or abolishes the affective component to pain, without disturbing pain threshold or pain intensity, 23 supporting the idea that affective components of pain are processed in different areas of the brain from sensation. Behavioral Factors. Suffering and pain are communicated through actions such as moaning, limping, grimacing, guarding, pill taking, or visiting the doctor. These actions are termed pain behaviors. Pain behaviors follow basic learning principles and tend to increase unconsciously if they are rewarded by positive consequences. Positive consequences may include attention from loved ones and/or the medical/dental

11 Nonodontogenic Toothache and Chronic Head and Neck Pains 297 system and avoidance of various aversive tasks and responsibilities. Since chronic pain conditions, by definition, last a long time, they provide an opportunity for unconscious learning to occur. The pain behaviors observed in a patient with chronic pain may be the cumulative result of intermittent positive reinforcement over months or years. In addition, well behaviors are often totally ignored and nonreinforced, causing them to decrease. Just as positive reinforcement causes an increase in particular behaviors, so will nonreinforcement cause a decrease. Thus, even when the nociceptive source has diminished or healed, pain perception and attendant disability may be maintained through learned pain behaviors along with physical, cognitive, and affective factors. 40 A more complete description of learned behavior in pain is given in the section on psychogenic pain. PAIN ASSESSMENT TOOLS Pain is a subjective experience that is communicated to us only through words and behaviors. Unlike measuring blood pressure, temperature, or erythrocyte sedimentation rate, measuring pain intensity is extremely difficult. As discussed above, there are several physiologic and psychological factors that will influence the intensity of pain perceived. Other cognitive, affective, behavioral, and learning factors affect how this pain is communicated. Nonetheless, measuring pain is important, not just for studying pain mechanisms in a laboratory but also to assess treatment outcome. To this end, a number of instruments have been developed and tested for their reliability and validity in measuring different aspects of the pain experience. Quantifying the Pain Experience Visual Analog Scales. A visual analog scale is a line that represents a continuum of a particular experience, such as pain. The most common form used for pain is a 10 cm line, whether horizontal or vertical, with perpendicular stops at the ends. The ends are anchored by No pain and Worst pain imaginable (Figure 8-13). Numbers should not be used along the line to ensure a better, less biased distribution of pain ratings. Otherwise, a disproportionately high frequency of 5s and 10s will be chosen. 41 Patients are asked to place a slash mark somewhere along the line to indicate the intensity of their current pain complaint. For scoring purposes, a millimeter ruler is used to measure along the line and obtain a numeric score for the pain ratings. Most people understand this scale quickly and can easily rate their pain. Children as young as 5 years are able to use this scale. 42 Its reliability and validity for measuring pain relief have been demonstrated. 43,44 The use of the scale should be clearly explained to the patient. For measuring treatment outcome, relief scales (a line anchored with no pain relief and complete pain relief ) may be superior to asking absolute pain intensities. 45 Similarly, if a pain intensity visual analog scale was used, patients may be more accurate if they are allowed to see their previous scores. 46 Caution is advised with photocopying because this process usually lengthens the line and introduces error. McGill Pain Questionnaire. The McGill Pain Questionnaire (Table 8-1) is a verbal pain scale that uses a vast array of words commonly used to describe a pain experience. Different types of pain and different diseases and disorders have different qualities of pain. These qualitative sensory descriptors are invaluable in providing key clues to possible diagnoses. Similarly, patients use different words to describe the affective component of their pain. To facilitate the use of these words in a systematic way, Melzack and Torgerson set about categorizing many of these verbal descriptors into classes and subclasses designed to describe these different aspects of the pain experience. In addition to words describing the sensory qualities of pain, affective descriptors including such things as fear and anxiety and evaluative words describing the overall intensity of the pain experience were included. 47 The words are listed in 20 different categories (see Table 8-1). They are arranged in order of magnitude from least intense to most intense and are grouped according to distinctly different qualities of pain. The patients are asked to circle only one word in each category that applies to them. Patients are usually happy to select from this list of pain-describing adjectives, often Figure 8-13 Visual analog pain scale used to indicate patient s level of daily pain. The patient places a mark at the perceived level of discomfort. The scale is 10 cm, so direct measurement can subsequently be made.

12 298 Endodontics Table 8-1 Sample of Classic McGill Pain Questionnaire Terms Describing Pain Sensory Flickering Jumping Pricking Sharp Pinching Quivering Flashing Boring Cutting Pressing Pulsing Shooting Drilling Lacerating Gnawing Throbbing Stabbing Cramping Beating Lancinating Crushing Pounding Tugging Hot Tingling Dull Tender Pulling Burning Itchy Sore Taut Wrenching Scalding Smarting Hurting Rasping Searing Stinging Aching Splitting Heavy Affective Tiring Sickening Fearful Punishing Wretched Exhausting Suffocating Frightful Gruelling Blinding Terrifying Cruel Vicious Killing Evaluative Miscellaneous Annoying Spreading Tight Cool Nagging Troublesome Radiating Numb Cold Nauseating Miserable Penetrating Drawing Freezing Agonizing Intense Piercing Squeezing Dreadful Unbearable Tearing Torturing saying, Now I can tell exactly how it feels. Before I couldn t think of just the right words. The first 10 categories represent different sensory descriptors that cover various temporal, spatial, pressure, and thermal qualities of pain. The next five categories are affective or emotional descriptors, category 16 is evaluative (ie, how intense is the pain experience), and the last four categories are grouped as miscellaneous. To score the questionnaire, the words in each category are given a numeric value. The first word in each category ranks as 1, the second as 2, etc. The scores for each category are added up separately for the sensory, affective, evaluative, and miscellaneous groupings. Then the total number of words chosen is also noted. Using this questionnaire, it is possible to obtain a sense of the quality of a patient s pain complaint (categories 1 through 10), its intensity (category 16), and the amount of emotional or psychological overlay accompanying the pain (categories 11 through 15). Changes in a patient s pain experience can be monitored by administering the questionnaire at various time points during treatment and follow-up. Melzack used this master list of words to derive quantitative measures of clinical pain that can be treated statistically; if used correctly, it can also detect changes in pain with different treatment modalities. 48 Psychological Assessment Chronic pain is the most complicated pain experience and the most perplexing and frustrating problem in medicine and dentistry today. Because chronic pain syndromes have such a complex network of psychological and somatic interrelationships, it is critical to view the patient as an integrated whole and not as a sum of

13 Nonodontogenic Toothache and Chronic Head and Neck Pains 299 individual parts. Determining the emotional, behavioral, and environmental factors that perpetuate chronic pain is as essential as establishing the correct physical diagnosis or, in many chronic cases, multiple diagnoses. Almost all patients with chronic head and neck pain have physical findings contributing to their complaint. Similarly, almost all patients with chronic head and neck pain have psychological components to their pain as well. Contributing to the complex neurobehavioral aspects of pain is the fact that chronic pain is not selflimiting, seems as though it will never resolve, and has little apparent cause or purpose. As such, multiple psychological problems arise that confuse the patient and perpetuate the pain. Patients feel helpless, hopeless, and desperate in their inability to receive relief. They may become hypochondriacal and obsessed about any symptom or sensation they perceive. Vegetative symptoms and overt depression may set in, with sleep and appetite disturbances. Irritability and great mood fluctuations are common. Loss of self-esteem, libido, and interest in life activities adds to the patient s misery. All of this may erode personal relationships with family, friends, and health professionals. Patients focus all of their energy on analyzing their pain and believe it to be the cause of all of their problems. They shop from doctor to doctor, desperately searching for an organic cure. They can become belligerent, hostile, and manipulative in seeking care. Many clinicians make gallant attempts with multiple drug regimens or multiple surgeries, but failure frustrates the clinician and adds to the patient s ongoing depression. Near the end of this progression, in addition to their continuing pain, many of these patients have multiple drug dependencies and addictions or high stress levels; they may have lost their jobs, be on permanent disability, or be involved in litigation. Herein lies the importance of proper psychological diagnosis as well as accurate physical diagnosis. An appropriate evaluation should include consideration of all factors that reinforce and perpetuate the pain complaints. Examining factors contributing to pain aggravation can include a look at stress (current and cumulative), interpersonal relationships, any secondary gain the patient may be receiving for having the pain, perceptual distortion of the pain, and poor lifestyle habits such as inadequate diet, poor posture, and lack of exercise. This information may well point to the reasons why patients have been unsuccessfully treated in the past. Obtaining baseline measures of pain levels, drug intake, functional impairment, and emotional state is important and will help monitor a patient s progress through rehabilitation. Systematic assessment of psychosocial difficulties that interfere with work and interpersonal activities is important but often neglected. The dentist should include questions to elicit information about oral habits, depression, anxiety, stressful life events, lifestyle changes, and secondary gain (operant pain) in the clinical interview. To decide which patient should be referred for a full psychological assessment, the clinician evaluating a patient with chronic pain may choose to use simple questionnaires that are easy to administer, do not take long to fill out, and are reliable and adequate psychological screening tools. The Multidimensional Pain Inventory (MPI), 49 Beck Depression Inventory (BDI/BDI-II),* 50,51 and Chronic Illness Problem Inventory (CIPI) 52 fulfill this purpose, although many other reliable instruments also exist. Patients who score high on any of these inventories should be sent to a psychologist or psychiatrist familiar with chronic pain for a more complete workup. Psychologists or psychiatrists may use the Minnesota Multiphasic Personality Inventory (MMPI/MMPI-II), 53 in addition to the BDI- II and other psychological instruments, as part of their comprehensive assessment. MAKING A DIAGNOSIS Diagnosing orofacial disease and headaches follows the same principles as any medical diagnosis. Of primary importance is a careful and exhaustive history. This alone will often point directly to a specific diagnosis or at least reveal a diagnostic category. The history is followed by a physical examination, which should help to confirm or rule out the initial diagnostic impression. If necessary, further diagnostic studies such as pulp testing, nerve blocks, radiographs, or blood tests may be carried out or ordered at this time. These may help rule out serious disorders and provide information complementing the history and physical examination. Finally, if doubt concerning the diagnosis persists, or pathosis out of one s area of expertise exists, other medical specialists and health care providers may provide valuable consultation. *The BDI and BDI-II can be obtained by contacting the Psychological Corporation, 555 Academic Court, San Antonio, TX Copies of the CIPI can be obtained by contacting Dr. Bruce Naliboff, PhD, Clinical Professor, Department of Psychiatry and Biobehavioral Sciences, Co-Director, CURE Neuroenteric Disease Program, UCLA Division of Digestive Disease, VA Greater Los Angeles Healthcare System, Building 115, Room 223, Wilshire Boulevard, Los Angeles, CA 90073; Tel: ; Fax

14 300 Endodontics Begin by pondering the scenario of the following case. Case History A 33-year-old woman presents herself for evaluation of intense left-sided facial pain. The pain is described as a constant burning sensation that radiates from the left preauricular area to the orbit, zygoma, mandible, and, occasionally, shoulder. Her pain is exacerbated by cold air, cold liquids, chewing, smiling, and light touch over certain areas of her face. She also reports a constant pinching sensation over her left eyebrow and mandible and photophobia in the left eye. She is currently taking high doses of narcotics with little relief. The pain began 1 year previously, after the extraction of a left maxillary molar. The extraction site apparently developed a dry socket (localized osteomyelitis of the alveolar crypt). This was treated appropriately but without relief of the patient s symptoms. Subsequently, two mandibular molars on the same side were extracted in an attempt to relieve the pain. These extraction sites likewise developed dry sockets and were treated, again without pain relief. Local anesthetic injections twice daily for many months and a 4-week course of cephalosporin, given empirically for possible periodontal infection or osteomyelitis of the mandible, were also unsuccessful. To properly evaluate these rather confusing signs and symptoms, additional information is necessary. Classification In evaluating orofacial pains and headaches, an easyto-use, practical, and clinical classification of these pains will facilitate diagnosis (Table 8-2). In developing such a classification, it is important to remember that local pathosis of the extracranial or intracranial structures and referred pain from pathema of more distant organs such as the heart must be ruled out first. This covers a wide variety of infectious, inflammatory, degenerative, neoplastic, or obstructive processes that can affect any organ in the head, neck, and thorax, including the brain (see Tables 8-7 through 8-9). Most dentists and physicians are well trained to evaluate a patient for such pathosis. There are other disorders, however, that cause pain in the head and neck region that cannot be attributed to any obvious diseases of the craniofacial, craniocervical, thoracic, or intracranial organs. These disorders are less well appreciated and, for ease of clinical use, are best classified according to the apparent tissue origin of the pain (see Table 8-2). For an exhaustive classification of headaches and facial pain that includes very specific diagnostic criteria, the reader is referred to the International Headache Society s publication. 54 The primary distinguishing feature of these diagnostic categories is the quality of the pain. For example, vascular pain, such as with migraine, generally has a throbbing, pulsing, or pounding quality; neuropathic pain, for example, trigeminal neuralgia, is usually described as sharp, shooting, or burning and is restricted to the peripheral distribution of the affected nerve branch; muscle pain is usually deep, steady, and aching or produces a sensation of tightness or pressure. In contrast, extracranial or intracranial pathema may present with any quality of pain. An inflamed tooth pulp may throb with each heartbeat. A tumor pressing on a nerve may cause sharp, lancinating, neuralgic-like pain. A sinus infection may be dull and aching. Referred pain tends to be deep and poorly localized and have an aching or pressing quality. Once organic pathosis has been ruled out, a preliminary diagnostic category can be chosen based on the Table 8-2 Practical Clinical Classification of Craniofacial Pain General Classification Origin of Pain Basic Quality of Pain Local pathosis of extracranial structures Craniofacial organs Any Referred pain from remote pathologic sites Distant organs and structures Aching, pressing Intracranial pathosis Brain and related structures Any Neurovascular Blood vessels Throbbing Neuropathic Sensory nervous system Shooting, sharp, burning Causalgic Sympathetic nervous system Burning Muscular Muscles Deep aching, tight Unclassifiable Etiology as yet unknown Any

15 Nonodontogenic Toothache and Chronic Head and Neck Pains 301 location and the quality of the pain. Therefore, when taking a pain history, the first questions to ask are Where, exactly, do you feel your pain? How, exactly, does your pain feel to you? Please mark on this line how severe you consider your pain to be at its worst, usual, and lowest. This will help guide further questioning to confirm or rule out a specific diagnosis within that group. For example, a patient may complain of a constant dull ache in front of the ear and a paroxysmal lancinating pain that shoots from the ear to the chin and tongue. In this situation, two patterns of pain are described. One points to a possibly myofascial or rheumatic diagnosis for the ear pain and the other to a paroxysmal neuralgia for the shooting pain. Further history, examination, and diagnostic tests will help establish more definitive physical diagnoses. This systematic approach is particularly helpful in chronic pain, in which there are often multiple diagnoses, and psychological distress and pain behavior may confuse the diagnostic process. If the patient in the case outlined above does not have any ongoing pathologic lesions of the extracranial or intracranial structures, which categories of pain would fit her description best? Based on the limited information given, namely, a constant burning quality, the most likely preliminary diagnostic categories are neuropathic or sympathetic. To make a specific diagnosis within a category, more specific information regarding the pain, its temporal pattern (timing of occurrence), associated symptoms, and aggravating and alleviating factors is needed. History The key elements of taking a history for a pain complaint are delineated in Table 8-3. Establishing the patient s chief complaint requires listening carefully as the patient describes each type of pain or complaint present, including the location, quality, and severity of each symptom. Chronic pain patients often have multiple pain complaints with different descriptions, which may indicate that multiple diagnoses are involved. When this is the case, obtaining complete information on each pain complaint separately simplifies the diagnostic process. The patient in the case scenario complains of only one pain. The location is over the left side of the face, radiating from the preauricular area. The quality of the pain is described primarily as burning. Her usual pain intensity on a 0 to 10 scale is 8, 5 being the lowest and 9 being the highest. Table 8-3 History of Pain Chief complaint Characteristics of pain Location Quality Temporal patterns Constant or intermittent Duration of each attack if intermittent Diurnal variation in intensity if constant Seasonal variation of symptoms if any Associated symptoms Precipitating factors if intermittent Aggravating factors Alleviating factors Symptoms severity range (lowest, usual, and highest pain intensities) Onset and history Past and present medications or other treatments for pain Past medical and dental history Family history Social history Review of systems Different pains also have different temporal patterns or patterns of occurrence. For example, a patient may complain of an intermittent, unilateral throbbing head pain. This would be the hallmark of a diagnosis in the vascular category. The exact pattern of the pain will help determine which vascular headache the patient is suffering. For example, migraines last from 4 to 48 hours and occur once or twice a year up to several times per month. Cluster headaches last less than 90 minutes each but occur several times a day, for several months, before going into remission. Similar distinctions can be made with neuropathic pains. The pain of trigeminal neuralgia is seconds in duration and may be triggered frequently throughout the day. The pain of a post-traumatic neuropathy or postherpetic neuralgia is constant. The temporal pattern for this patient s burning pain is constant, with little daily variation. Often there are associated symptoms such as nausea, vomiting, ptosis, nasal congestion, tingling, numbness, blurred vision, or visual changes that may precede or accompany the pain. These symptoms may point to a specific diagnosis. For example, visual changes may precede a migraine with aura. Nausea and vomiting often accompany severe headaches, especially migraine.

16 302 Endodontics Generalized malaise may accompany a temporal arteritis. Autonomic changes, such as ptosis, nasal congestion, or conjunctival injection, almost always accompany cluster headaches or chronic paroxysmal hemicrania. Tingling and numbness may occur with deafferentation (nerve damage) pains such as postherpetic or post-traumatic neuralgias. Unexplained neurologic symptoms, however, such as cognitive or memory changes, transient sensory or motor loss of the face or extremities, tinnitus, vertigo, loss of consciousness, or any of the above symptoms not fitting an appropriate pain picture, must alert the health professional to the possibility of an intracranial lesion, requiring further workup. Some of these symptoms may be normal bodily sensations enhanced through distorted perceptions. Similarly, others, such as tinnitus, vertigo, or sensory tingling, may be associated with the referred symptoms of myofascial TrP pain. 55 Further diagnostic tests or consultations may be needed to rule out more serious pathosis. Associated symptoms for this patient include a constant pinching sensation over her left eyebrow and mandible and photophobia of the left eye. She also describes occasional electric attacks that radiate out from the left TMJ. The electric attacks she describes last anywhere from 30 minutes to 24 hours. Precipitating, aggravating, and alleviating factors also add clues to the origin of pain. Foods rich in tyramine may trigger a migraine attack. 56 Light touch, shaving, or brushing teeth may precipitate an attack of trigeminal neuralgia. Cold weather, maintaining any one body position for a prolonged period of time, or overexercise will aggravate MFP. A dark room and rest will alleviate migraine but aggravate cluster headache. Heat and massage will alleviate muscular pain and MFP but may aggravate an inflamed joint. The burning pain is constant, without precipitating factors. Aggravating factors include cold air, cold liquids, chewing, smiling, and light touch. The electric attacks are precipitated by light touch over the preauricular area. At this stage, nothing alleviates the pain. High doses of narcotics barely serve to take the edge off. Gathering information about the onset and history of the problem will provide further clues as to the etiology of the complaint. Of interest are the events surrounding the initiation of the pain, how the pain has changed since onset, and what evaluations and treatment have been tried in the past. For example, a history of skin lesions and malaise (herpes zoster) typically precedes postherpetic neuralgia. Acute trauma may precede a myofascial TrP pain complaint. In contrast, psychological stress can trigger almost any type of pain complaint. Knowing which specialists the patient has seen, which tests and radiographs have already been completed, what the previous diagnostic impressions have been, and which treatments have been tried helps the practitioner in several ways. First, which workups are still needed? Did the past workups adequately rule out organic or life-threatening pathema? How long ago were these workups completed? Have the symptoms changed since then? Do any of these workups need to be repeated? Second, what diagnoses were considered in the past? Were appropriate medications or treatments tried, in adequate doses and for long enough periods of time? With acute pain, the history is usually quite short, but with chronic pain, the history may take hours to obtain, the patient having seen many different health care providers in the past. With chronic pain, the effect of past medications, surgeries, and other treatments may provide insight not only into the etiology of the pain but also the psychological or behavioral status of the patient. The pain began 1 year previously, after the extraction of a left maxillary molar. The extraction site apparently developed a dry socket. This was treated appropriately but without relief of the patient s symptoms. Subsequently, two left mandibular molars were extracted in an attempt to relieve the pain. These extraction sites likewise developed dry sockets and were treated, again without pain relief. Local anesthetic injections twice daily for many months and a 4-week course of cephalosporin given empirically for possible periodontal infection or osteomyelitis of the mandible were also unsuccessful. This history tells us that, initially, local tooth pathosis was suspected as the etiology of the pain. However, extraction of teeth provided no relief. Osteomyelitis and possibly periodontal disease had also been suspected, but high-dose antibiotic treatment for osteomyelitis also failed to provide pain relief. Are there other extracranial or intracranial pathemas that may need to be ruled out? A family history should include information regarding the patient s parents and siblings. Are they alive and

17 Nonodontogenic Toothache and Chronic Head and Neck Pains 303 well? If not, why not? Does anyone in the immediate family suffer from a similar pain problem? For example, 70% of migraine patients have a relative who also has or had migraine. Does anyone in the family have a chronic illness? This person may provide a model for pain behavior and coping. The patient s parents and siblings are alive and well. There is no history of similar illness or chronic illness in her family. A social history not only should cover demographic information, marital status, household situation, and occupation but should also seek to uncover any potential perpetuating factors to the pain. Look for potential stressors at work and at home and ask about postural habits, body mechanics, dietary habits, environmental factors, and drug and alcohol use. This patient lives in a rural farm area, has been married to the same man for 15 years, and has three children. She used to work on the farm but has been unable to do so for the last 6 months because of the pain. The patient has smoked one pack a day for 18 years. She does not drink alcohol. Currently she spends most of her day in bed because of the pain. Since the patient lives in a rural area, the possibility of a coccal infection must be considered and ruled out. The past medical history may reveal some underlying illness such as lupus erythematosus or hypothyroidism that may predispose the patient to developing pain. Past surgeries and medications for other purposes, any psychiatric history, allergies, hospitalizations, and other illnesses must be included and may reveal health care abuse. The patient states that she is otherwise in good health. She had the usual childhood diseases, has no known allergies, and has been hospitalized only for the birth of her children. There is no history of trauma other than the tooth extractions previously mentioned. A review of systems screens the person s present state of health. It includes asking about any recent symptoms related to the head and neck; the skin; and the cardiovascular, respiratory, gastrointestinal, genitourinary, endocrine, neurologic, obstetric-gynecologic, and musculoskeletal systems. The patient complains of decreased energy and sleep disturbance secondary to the pain. She has no other complaints. In acute pain problems, a firm diagnosis may be established almost immediately from the history. In contrast, diagnosis of a chronic pain complaint may take months of tests or trials despite an exhaustive history. The next step in diagnosis is a thorough physical examination. Physical Examination The physical examination for craniofacial pain may vary slightly, depending on its location and the apparent cause. Pathosis of extracranial structures, particularly the oral cavity, must be sought and ruled out first. This usually involves inspection, palpation, percussion, transillumination, and auscultation of the tissues and structures suspected of causing pain. Intraoral examination, which must include inspection of all intraoral tissues, teeth, and periodontium, is discussed in detail in chapters 6 and 7. Once acute pathema has been ruled out, the physical examination must be augmented to include evaluation of the cranial nerves, temporomandibular joint, cervical spine, and head and neck muscles. In specific cases, a more comprehensive neurologic examination may be indicated. The basic components of a physical examination are listed in Table 8-4. General inspection can reveal a great deal about a patient to the alert clinician. A slouching posture can point to depression. Rigidity in posture or clenching is an indication of excess muscle tension in the neck, shoulders, or jaws. Asymmetry, swelling, redness, and other signs may indicate a neoplastic or infectious process. Closer inspection of the head and neck may reveal scars of past surgeries, trophic skin changes associated with reflex sympathetic dystrophy, or color changes from local infection, systemic anemia, or jaundice. The examination of the TMJs involves testing the range and quality of motion of the mandible, palpating and listening for joint noises, and palpating the lateral Table 8-4 Physical Examination General inspection Head and neck inspection Stomatognathic examination Cervical spine examination Myofascial examination Cranial nerve examination Neurologic screening examination

18 304 Endodontics and dorsal joint capsules for tenderness. The normal range of jaw opening is 40 to 60 mm. Laterotrusive and protrusive movements should be 8 to 10 mm. The path of opening and laterotrusive and protrusive movements should be straight, without deflections or deviations. Joint capsule palpation anterior to the tragus of the ear for the lateral capsule and from the external auditory meatus for the dorsal capsule may be uncomfortable but should not be painful. As discussed later in the chapter, the cervical spine is often the source of persistent referred pain to the orofacial and TMJ regions. Similarly, poor posture is one of the most important contributing factors to TMJ dysfunction and myofascial TrP pain. For these reasons, the cervical spine and posture must be evaluated in any chronic head and neck or facial pain problem. Examination of the cervical spine includes testing its range and quality of motion as a whole, as well as testing the range and quality of motion of the first two cervical joints individually Posture, especially anterior head positioning, must also be systematically evaluated. For details on how and why this is important, the reader is referred to Travell and Simons Trigger Point Manual. 55 Myofascial TrP examination requires a thorough, systematic palpation of all of the masticatory and cervical muscles, looking for tight muscle bands and the focal tenderness associated with myofascial TrPs. Myofascial TrP is the most prevalent cause of chronic pain, both in the head and neck region and in general Also, it is frequently an accompanying diagnosis to other chronic pain conditions. A cranial nerve examination (Table 8-5) is indicated when the history points to a neuropathic type of pain; if disturbances in touch, taste, smell, sight, hearing, motor function, balance, or coordination are suspected; or if there are any subjective complaints or objective signs of cranial nerve involvement. Lesions of the cranial nerve nuclei or their efferent or afferent pathways will result in an abnormal examination. For example, meningitis may cause double vision; an acoustic neuroma may cause hearing loss. Symptoms of numbness or tingling may accompany nasopharyngeal carcinoma or other intracranial pathema. Sensory deficits can be verified using accurate two-point discrimination testing, pinprick tests, and light touch tests. Complaints of transient or persistent paralysis, weakness, or spasticity of any of the head and neck muscles dictate the need for evaluation of the nerves that control their motor function. The motor function of the head and neck is mediated through several cranial nerves. The trigeminal nerve, cranial nerve V, controls the masticatory mus- Table 8-5 Cranial Nerve Examination I. Olfactory Test sense of smell of each nostril separately by using soap, tobacco, or coffee with patient s eyes closed II. Optic Test visual acuity Examing fundi ophthalmoscopically Test visual fields III, IV, VI. Oculomotor, Trochlear, Abducens Test pupillary reactions to light and accommodation Test extraocular movements Check for ptosis or nystagmus V. Trigeminal Motor Palpate masseter and temporalis during contraction Sensory Test discrimination of pinprick, V1, V2, V3 temperature, V1, V2, V3 and light touch, V1, V2, V3 Test corneal reflex VII. Facial Observe patient s face during rest and conversation Check for symmetry, tics Examine for symmetric smile, ability to wrinkle forehead, hold air in cheeks, and tense the platysma muscle VIII. Acoustic Whisper, rub fingers or hold watch next to ear, use tuning fork for Rinne & Weber tests IX, X. Glossopharyngeal, Vagus Check for symmetric movement of soft palate and uvula when patient says Ah Check gag reflex by touching back of throat Note any horseness XI. Spinal accessory Have patient shrug shoulders against resistance (trapezius) (partially inervated by C4) Have patient turn head against resistance (SCM) XII. Hypoglossal Observe tongue in mouth: check for atrophy or asymmetry Check for deviation by having patient stick tongue out

19 Nonodontogenic Toothache and Chronic Head and Neck Pains 305 cles. The facial nerve, cranial nerve VII, controls the muscles of facial expression. The hypoglossal nerve, cranial nerve XII, controls the tongue. The spinal accessory nerve, cranial nerve XI, controls the trapezius and sternocleidomastoid muscles. Detailed information on how to perform a cranial nerve examination is available in Bates s textbook on physical examination and history taking. 65 If intracranial pathosis is suspected, a complete neurologic examination, including mental status; cerebellar, motor, and sensory function; and reflexes, is indicated. This requires referral to a competent neurologist. General inspection of the patient reveals an obese female in moderate distress. Closer inspection of the head and neck reveals slight swelling of the left cheek with a distinct increase in skin temperature over this site. On intraoral examination, the intraoral tissues are firm, pink, and stippled without lesions. The patient is missing teeth #15, 16, 17, 18, and 19. Temporomandibular joint examination reveals an active oral opening of only 33 mm with little translation of the left condyle (the jaw deflects to the left with opening). Definitive intraoral or extraoral palpation is impossible because the patient complains of pain at the slightest touch. The patient has full range of motion of the cervical spine. The first two cervical joints similarly show good range and quality of motion. Her posture is slightly abnormal, with elevation of the left shoulder and a forward head position. Myofascial TrP examination is restricted to the cervical muscles and unaffected side owing to the extreme sensitivity of the left side of the face. Even so, active myofascial TrPs are found in the left upper trapezius that intensify the patient s pain over the left temple and angle of the jaw. Cranial nerve examination is normal except for the extreme cutaneous sensitivity on the left side of the face. Neurologic examination is similarly unremarkable. At this stage, one must still rule out acute pathologic change. Pathosis of the various organs and structures of the head and neck should always be suspected first in any orofacial pain. The teeth, pulp and periodontium, TMJs, eyes, ears, nose, throat, sinuses, and salivary glands should be thoroughly evaluated (see Table 8-7). As mentioned previously, the quality of pain from this group varies depending on the etiology. Equally important are many referred pain problems (see Table 8-8). These are very often difficult to diagnose and include pathologic conditions such as the tight, pressing pain of coronary artery disease that may be felt in the sternum and the jaws. This patient demonstrates swelling and temperature change as well as cutaneous hyperesthesia over the painful area. She could still have a chronic osteomyelitis despite the previous course of antibiotics. She could have a retropharyngeal abscess or neoplastic disease affecting or surrounding the fifth cranial nerve, either intracranially or extracranially. She could also have a localized coccal infection since she lives in a rural area. The limited range of motion of the left temporomandibular joint and the fact that much of her pain seems to emanate from there bring up the possibility of severe degenerative joint disease or neoplastic disease involving the joint. The myofascial TrPs in the left trapezius have probably developed in response to the chronic pain problem. It is unlikely that myofascial TrP pain is the primary cause of this patient s pain. The next step involves choosing appropriate diagnostic studies to help rule out the pathema suspected. Diagnostic Studies Table 8-6 is a list of some of the more common diagnostic studies available to help facilitate diagnosis. Panoramic and periradicular radiographs reveal an area of bony sclerosis in the mandibular extraction sites, consistent with the history of curettage of dry sockets and not at all typical of osteomyelitis. Temporomandibular joint tomograms reveal flattening of the left condyle consistent with mild to moderate degenerative joint disease. Computed tomographic (CT) scans of the brain, mandible, and retropharyngeal area are normal. A gallium scan, which is used to identify soft tissue inflammation, is normal also. Skin tests for coccal infection are negative. Complete blood count and erythrocyte sedimentation rate also fail to show any signs of infection or inflammation. No pathosis of the extracranial and intracranial structures can be identified. What, then, could be causing this patient s pain? At this point in the workup of a pain patient, practitioners are often tempted to ascribe the pain to some psychogenic problem. Clearly, if there is no obvious pathologic process, and the patient is in severe distress or does

20 306 Endodontics Table 8-6 Common Diagnostic Studies Pulp testing Radiography Tomography Laboratory studies (blood, urine) CT or MRI scan Bone scan Gallium scan Arthrography Thermography Nerve conduction studies EEG Lumbar puncture Differential diagnostic analgesic blocking not respond well to treatments, then she must be suffering from a psychogenic pain. Don t be too sure! Psychogenic Pain Many clinicians use the term psychogenic to refer to patients with a chronic pain problem that has a strong emotional component or to patients who do not respond well to somatic treatment. It must be reemphasized, however, that psychological factors are intimately involved in the expression of all pain, regardless of etiology or time course. By definition, chronic pain has been present for a protracted period (at least 6 months), and the patient has usually received multiple treatments with little or no results. This creates an emotional strain for the patient and frustration for the clinician, sometimes resulting in the inappropriate label of psychogenic pain. Patients with chronic pain invariably have a somatic diagnosis. What frustrates the clinician is often the discrepancy between the identifiable somatic cause and the disproportionate amount of perceived pain and disability that accompanies this cause. True psychogenic pain is a rare diagnosis that must be restricted to those patients in whom thorough, sophisticated medical evaluations and tests fail to uncover any somatic basis for their pain and in whom psychological evaluation reveals psychopathology that may actually account for their presentation. Myofascial TrP pain is frequently overlooked as an organic finding and is thus often mislabeled as psychogenic pain. 66 Occasionally, there are patients in whom no etiology for their pain can be identified and who have no psychological findings consistent with a psychological disorder. This situation simply speaks to the limitations of our current medical knowledge and the complexity of the human nervous system and is not an indication of the mental state of the patient. Conversion Reaction. A true conversion reaction is very rare. It is thought to represent the successful substitution of a more valid somatic symptom for emotional turmoil in a patient s life. This symptom is most frequently blindness or deafness, and the condition is more common in young women. 67 However, patients can be of any age or sex, and, occasionally, the symptom substitution may involve pain. When this occurs, the quality of the pain can be related in very descriptive, affective terms such as lightning-like explosions, heavy weight pressing on my head, spike into my head, rope choking my throat, ugly pain, and others. The pain is usually described as continuous or unrelenting. It is rarely affected by external events; however, it can be changed by emotions. Despite the elaborate terms used to describe the pain, these patients often appear indifferent about it. Clinically, there are usually no physical findings, including no myofascial TrPs. A careful history may reveal that patients either grew up with a parent or relative who was ill or they themselves had a history of a prolonged childhood illness. Mental status may be normal; however, these patients generally have been and are under intense emotional stress, have poor social relationships, and may be occupationally incapacitated. The reasons for a conversion reaction vary. Causes may include handling nonspecific stress, anticipating a major life change, dealing with a catastrophic life situation, and the manifestation of a severe body image problem. The patient subconsciously converts an apparently socially unacceptable psychological illness to the socially acceptable physical complaint of pain. Somatic Delusions. Somatic delusions may occur in patients with psychiatric diagnoses such as psychosis or schizophrenia. These patients lose rational thought and attachment to reality and display uncontrolled obsessions of pain or problems with their health. Psychiatric care or hospitalization is strongly indicated since the possibility of suicide may be great. Operant Pain (Pain Behavior). Although pain behaviors (the behavioral manifestations of pain, distress, and suffering) likely result from a complex interaction of various psychological and physical factors, 40 understanding the basic concepts of learning and operant conditioning is essential to understanding the chronic pain patient. In combination with cognitive and affective factors, learned behavior and operant conditioning are powerful psychological or psychogenic factors that play