Chapter 8 NONODONTOGENIC TOOTHACHE AND CHRONIC HEAD AND NECK PAINS Bernadette Jaeger Pain is perfect misery, the worst of evils; and excessive, overturns discomfort, distress, or agony resulting from the stim- all patience. ulation of specialized nerve endings.”1 In this defini- –John Milton, Paradise Lost tion, the behavioral reaction to nociception is already assumed to be distress or agony, which is not always Patients with chronic oral or facial pain, or headache, the case. Take, for example, the observations made by present a true diagnostic and therapeutic challenge to Beecher in 1956 that only 25% of soldiers wounded in the practitioner. For many in the dental profession, the battle requested narcotic medications for pain relief, only solution to problems of pain lies with a scalpel, for- compared to more than 80% of civilian patients with ceps, or ever-increasing doses of analgesics, narcotics, or surgical wounds of a similar magnitude.2 Clearly, the sedatives. Many patients with chronic pain have suffered behavioral reaction to similar nociceptive stimuli this mistreatment and stand as an indictment of a poor- varies from person to person and depends on a num- ly trained, insecure, and disinterested segment of den- ber of factors, including the significance of the injury tistry. Attending to patients who have been unable to to that individual. The wounded soldier may be obtain resolution of their pain complaint, despite exten- relieved to be out of a life-threatening situation; the sive evaluation and treatment, requires a compassionate surgical patient may be concerned about recurrence of reappraisal and fresh approach. Fortunately, accurate a tumor just removed. Dorland’s definition also diagnosis and successful management of these patients implies that stimulation of nociceptors is required for can be among the most rewarding experiences in dental perception of pain, yet the dental patient who has been or medical practice. anxious for weeks in anticipation of the “needle” at the dentist’s office may jump in agony at the slightest WHAT IS PAIN? touch of his cheek. Pain is not a simple sensation but rather a complex Fields defined pain as “an unpleasant sensation that neurobehavioral event involving at least two compo- is perceived as arising from a specific region of the body nents. First is an individual’s discernment or percep- and is commonly produced by processes that damage tion of the stimulation of specialized nerve endings or are capable of damaging bodily tissue.”3 He empha- designed to transmit information concerning potential sized the need to be able to localize the painful source or actual tissue damage (nociception). Second is the in order to distinguish it from psychological pain and individual’s reaction to this perceived sensation (pain suffering, for example, the “pain” of a broken heart. behavior). This is any behavior, physical or emotional, A more complete definition is cast by the that follows pain perception. Culture or environment International Association for the Study of Pain (IASP) often influences these behaviors. Beyond this is the suf- in its taxonomy of painful disorders.4 That definition fering or emotional toll the pain has on any given indi- of pain is as follows: “An unpleasant sensory and emo- vidual. Suffering is so personal that it is difficult to tional experience associated with actual or potential quantify, evaluate, and treat. tissue damage, or described in terms of such damage.” The fact that pain is difficult to define, quantify, and Added to this definition, however, is the following, understand is reflected in the numerous ways in which emphasizing the subjective nature of pain that distin- it has been described. Dorland’s Medical Dictionary guishes and separates it from the simple stimulation of defines pain as “a more or less localized sensation of nociceptors: 288 Endodontics Pain is always subjective. Each individual learns To understand pain better, this chapter first looks at the application of the word through experiences what is currently known about the anatomy and phys- related to injury in early life. It is unquestionably a iology of the nociceptive pathways and some of the sensation in a part of the body, but it is also always modulating influences that modify the nociceptive unpleasant and therefore also an emotional expe- input into the central nervous system. Following this, rience. Many people report pain in the absence of various psychological and behavioral factors that influ- tissue damage or any likely pathophysiological ence the perception of and reaction to pain are cause, usually this happens for psychological rea- reviewed. sons. There is no way to distinguish their experi- ence from that due to tissue damage, if we take the NEUROPHYSIOLOGY OF PAIN subjective report. If they regard their experience as The following summarizes what is known about the pain and if they report it in the same ways as pain basic anatomy and physiology of pain under normal caused by tissue damage, it should be accepted as physiologic conditions5: pain. This definition avoids tying pain to the stim- ulus. Activity induced in the nociceptor and noci- Acute Pain Pathways ceptive pathways by a noxious stimulus is not pain, The body has specialized neurons that respond only to which is always a psychological state, even though noxious or potentially noxious stimulation. These neu- we may well appreciate that pain most often has a rons are called primary afferent nociceptors and are proximate physical cause.4 made up of small-diameter thinly myelinated A delta and unmyelinated C fibers (Figure 8-1). They synapse The IASP definition of pain makes the point that in the substantia gelatinosa of the dorsal horn of the pain is pain even if a nociceptive source is not readily spinal cord with neurons known as second-order pain identified. Pain owing to psychological causes is as real transmission neurons. From here the signals are trans- as any pain associated with actual nociception and mitted along specialized pathways (spinothalamic and should be treated as such. reticulothalamic tracts) to the medial and lateral 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), small- diameter 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 A 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): 1975. B Nonodontogenic Toothache and Chronic Head and Neck Pains 289 regions of the thalamus (Figure 8-2). Perception of nociceptor. Bradykinin further contributes by causing nociception may occur in the thalamus and cortex, but the sympathetic nerve terminal to release a the exact location is unknown, and the contribution of prostaglandin that also stimulates the nociceptor.6 the cortex to pain perception is controversial.3 Additionally, in an area of injury or inflammation, the Fields divided the processing of pain from the stimu- sympathetic nerve terminal will release yet another lation of primary afferent nociceptors to the subjective prostaglandin in response to its own neurotransmitter, experience of pain into four steps: transduction, trans- norepinephrine. The presence of such an ongoing mission, modulation, and perception.3 Transduction is inflammatory state causes physiologic sensitization of the activation of the primary afferent nociceptor. the primary afferent nociceptors.6 Sensitized nocicep- Primary afferent nociceptors can be activated by intense tors display ongoing discharge, a lowered activation thermal and mechanical stimuli, noxious chemicals, threshold to normally nonpainful stimuli (allodynia), and noxious cold. They are also activated by stimula- and an exaggerated response to noxious stimuli (pri- tion from endogenous algesic chemical substances mary hyperalgesia).7 (inflammatory mediators) produced by the body in In addition to sending nociceptive impulses to response to tissue injury. Damaged tissue or blood cells synapse in the dorsal horn of the spinal cord, activation release the polypeptide bradykinin (BK), potassium, of cutaneous C fibers causes their cell bodies to synthe- histamine, serotonin, and arachidonic acid. Arachidonic size the neuropeptides, substance P and calcitonin acid is processed by two different enzyme systems to gene–related peptide (CGRP). These neuropeptides produce prostaglandins and leukotrienes, which, along are then antidromically transported along axon with BK, act as inflammatory mediators (Figure 8-3). branches to the periphery by an axon transport system Bradykinin acts synergistically with these other chemi- where they induce further plasma extravasation and cals to increase plasma extravasation and produce increase inflammation. The release of these algogenic edema. Plasma extravasation, in turn, replenishes the substances at the peripheral axon injury site produces supply of inflammatory chemical mediators. Whereas the flare commonly seen around