OROFACIAL PAIN

V CHRONIC PAIN: NONCANCER PAIN 121

Chapter 17

OROFACIAL PAIN Rafael Benoliel, Richard A. Pertes, and Eli Eliav

INTRODUCTION Orofacial pain includes, by definition, pain that originates from oral structures accompanied by facial pain. The facial area includes the region demarcated as below the orbitomeatal line, above the neck, and anterior to the ears. However, the craniofacial region has a high density of anatomic structures, and pain often radiates from one area to the other. As a result, the patient with orofacial pain may seek help from a number of specialists. The prevalence of orofacial pain is around 17% to 26%, out of which 7% to 11% is chronic.1 Most patients, therefore, suffer acute pain that is in the most part secondary to dental or intraoral soft tissue pathology. Epidemiologic data on dental pain are sparse and of poor quality, and its reported prevalence in community dwelling adults ranges from 12% to 40%, depending on the description of dental pain used. Chronic orofacial pain is most frequently due to musculoskeletal pain, but neuropathic and neurovascular pains are also encountered.

DENTAL PAIN Dentinal Pain (see Table 17–1) The pain originating in dentine is sharp, deep, and usually evoked by external stimuli: hot, cold, sweet, sour, and sometimes, salty foods and drinks. The pain generally subsides within a few seconds. Extreme temperatures (hot soup or ice cream) may cause pain in healthy or restored teeth, but this is often mild and transient. The most common processes associated with dentine pain are early dental caries, defective restorations, and areas of exposed dentine (e.g., abrasion or erosion of the enamel) and exposed roots (due to gingival recession). Diagnosis is by direct observation and examination with a sharp dental probe, augmented by the use of dental radiographs.

The Cracked-tooth‘‘Syndrome’’ A cracked tooth induces sharp pain after biting that resolves immediately after pressure on the tooth ceases. Localization to the affected area of teeth is good, but identification of the exact tooth is imprecise. The patient may have pain and discomfort associated with cold and hot stimuli in the area. Diagnosis is by percussion or pressure on the cusps of the suspected teeth at different angles and by asking the patient to bite on individual cusps using a Ene wooden stick or a predesigned bite stick (available commercially). Probing of Essures and, if the tooth is restored, the margins of restorations may aid in identifying fractures.

Treatment of Dentinal Pain (see Table 17–1)

ACUTE OROFACIAL PAIN Most frequently, dental pain is due to dental caries, although a broken filling or tooth abrasion may also cause dental sensitivity. Other oral pains are periodontal or gingival in origin (Tables 17–1 to 17–4). Acute dental and periodontal pain is moderate to severe in intensity (6–10 on a 10-cm visual analog scale [VAS]). In about 60% of cases, pain is hard to localize but spreads into remote areas of the head and face; periodontal pain, however, is usually localizable. There is considerable overlap in pain referral patterns for maxillary and mandibular sources, and the extent of referral to adjacent facial structures positively correlates with pain intensity. Generally, a connection exists between caries extent and the presenting symptomatology. Initial caries, located in the superficial layer of the dentine, induces tooth sensitivity to various stimuli such as change in temperature and sweet substances. Pain is usually not spontaneous. As the lesion penetrates, pain produced by these stimuli becomes both stronger and prolonged. Eventually, when the caries affects the tooth pulp, strong, spontaneous, paroxysmal pain develops that is usually intermittent in nature. As the root apex is invaded by bacterial and tissue disintegration by-products, the tooth becomes very sensitive to chewing, touch, and percussion. At this point, pain generally becomes continuous and the tooth is no longer sensitive to changes in temperature. In clinical practice, however, the demarcation between these various stages may overlap and the tooth may be sensitive simultaneously to temperature changes and to chewing.

Removal of the carious lesion and restoration of the tooth with plastic restorative materials generally resolve symptoms. Sensitivity usually disappears within a day or two, but it may persist (weeks) when the carious lesion is deep. Treatment of the cracked tooth depends on the state of the tooth (existing restorations, periodontal condition) and the extent of the fracture. Existing restorations associated with tooth fractures can be replaced with adhesive restorative materials; these may be successful but are associated with postoperative sensitivity. Often, cracked teeth require crowning. Exposed cervical dentine may be hypersensitive to thermal stimuli and toothbrushing in the area. Acidic foods or beverages frequently enhance dentinal sensitivity. Desensitizing toothpastes with ingredients such as stannous fluoride or potassium nitrate will improve symptoms for most cases, or a variety of physical and chemical agents applied by the dentist are able to induce a smear layer or block the tubules. Tubule-blocking agents include resins, glass ionomer cements and bonding agents; strontium chloride or acetate; aluminium, potassium, or ferric oxalates; silica- or calciumcontaining materials; and protein precipitants.

Pulpal Pain (see Table 17–2) Pulpal pain is spontaneous, strong, often throbbing, and exacerbated by changes in temperature, sweet foods, and pressure on the carious lesion. Evoked pain outlasts the stimulus for a number of minutes (unlike stimulus-induced dentinal pain) and can be excruciating. Localization is poor and becomes poorer as pain severity increases. Pain originating from the pulp is not usually

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Table 17^1. Current Diagnosis and Therapy of Dentinal Pain Primary Diagnosis Pain Intensity Location

Clinical Symptoms

Examination Findings

Radiography

Treatment

Mild to moderate

Locally Adjacent around teeth affected tooth

Sensitivity to sweet and thermal stimuli

Faulty restorations, carious lesion

Caries, exposed dentine

Exposed Mild to cervical moderate dentine Cracked Mild to tooth moderate

Adjacent Locally teeth around affected tooth Locally Localized around affected tooth

Sensitivity to cold and to toothbrushing Sensitivity to biting on tooth or chewing in the area

Gingival recession, exposed sensitive dentine Pain on pressure to tooth cusp

Not relevant

Removal of caries, restoration of tooth Desensitization

Caries

Referral

continuous and abates spontaneously; the precise explanation for such abatement is unclear. Pain may increase and throb when the patient lies down and, in many instances, wakes the patient from sleep. In some cases, pain may be continuous and dull, periodically exacerbated (by stimulation or spontaneously) for short (minutes) or long (hours) periods. When the pain is episodic, sharp, and paroxysmal, it may be confused with other conditions that mimic pain of pulp origin such as trigeminal neuralgia (TN). Application of ethyl chloride on a pledget of cotton wool usually induces a short, mildly painful response from intact teeth. The pulpal condition may be reversible or irreversible. In reversible pulpitis, pain response is increased (hyperalgesia) and outlasts the stimulus, usually by less than 10 seconds. In irreversible pulpitis, application of ethyl chloride results in excruciating pain that outlasts the stimulus for well beyond 10 seconds. Percussion aids in localizing the tooth with painful pulpitis; 80% are tender to percussion. Nonvital pulps do not react to cold application.

Not relevant

Removal of fractured material and restoration or tooth crowning

Depending on the diagnosis, treatment may aim at conserving the pulp, extirpating it, or extracting the tooth. Pulpal pain normally disappears immediately after treatment. Irreversible pulpitis dictates endodontic therapy or extraction. Normal pulpal vitality and no pain to percussion indicate that the diagnosis is reversible pulpitis. The tooth pulp may be preserved by caries removal with indirect pulp capping and the use of mild analgesics.

PERIODONTAL PAIN (see Table 17–3) The periodontal tissues include the alveolar bone, the periodontal ligament, and the gingivae. A major feature of chronic periodontal disease is that it is generally painless. Pain originating in the periodontal structures is easily localized; the affected teeth are very tender on chewing and are readily identified by percussion. Periodontal pain usually results from an acute inflammatory

Table 17^2. Current Diagnosis and Therapy of Pulpal Pain Diagnosis

Pain Intensity

Reversible pulpitis

Moderate to severe

Irreversible Severe pulpitis

Primary Location

Referral

Poorly localized Adjacent teeth to the affected jaw

Very poorly localized to the affected jaw

Opposing jaw, temple

Clinical Symptoms

Examination Findings

Radiography

Restoration in Large, faulty restoration. Large proximity to carious lesion or dental pulp exposed pulp. Hypersensitive to cold application. Deep carious Large, faulty Severe lesion. continuous or restoration Large carious paroxysmal lesion or exposed pain pulp Hypersensitive Extremely to cold and sometimes to hypersensitive to cold application biting on the with pain tooth outlasting stimulus by > 10 sec Hypersensitive to thermal stimuli

Treatment

Tooth may be amenable to conservative therapy: new restoration, repair Pulp extirpation or tooth extraction

V CHRONIC PAIN: NONCANCER PAIN 123

Table 17^3. Current Diagnosis and Therapy of Periodontal Pain Diagnosis

Pain Primary Intensity Location

Periapical Severe periodontitis

Localized to tooth

Severe

Localized to tooth

Lateral periodontal abscess

Referral

Clinical Symptoms

Examination Findings Radiography

Affected tooth not Adjacent teeth, Pain on chewing or approximating teeth vital opposing Extreme tenderness to jaw, ipsilateral May be associated percussion on the with intra- or temple, affected tooth extraoral swelling regional Hypersensitivity in (DAA) lymph nodes soft tissue overlying apical area Swollen tender regional lymph nodes Adjacent teeth, Pain on chewing Tooth may be vital opposing Intraoral swelling Deep periodontal jaw, ipsilateral pocket temple, Associated soft tissue regional swelling: usually lymph nodes located more coronally than in DAAs

Deep restoration, deep caries Old root canal therapy May or may not be associated with a periapical radiolucency Usually generalized periodontal disease A radiolucency may be observed in the lateral periodontal space

Treatment

De´bridement of pulp chamber and canals Redo root canal therapy May require antibiotic therapy

Curettage and irrigation of pocket If tooth pulp affected, may need extirpation or de´bridement Antibiotic therapy

DAA, dentoalveolar abscess.

process of the gingivae, the periodontal ligament, and alveolar bone due to bacterial or viral infection.

Acute Periapical Periodontitis Pain associated with acute periapical inflammation is spontaneous, of moderate to severe intensity, and long lasting (hours). Pain increases with biting on the affected tooth and, in more advanced cases, even with closing the mouth and bringing the tooth into contact with the opposing teeth. In these cases, the tooth feels extruded and is very sensitive to touch. Frequently, the patient reports symptoms of pulpal pain that preceded pain from the periapical area. Localization of pain originating from the periapical area is usually precise, and the patient is able to indicate the affected tooth. The affected tooth is readily located by means of gentle tooth percussion, and the periapical vestibular area may be tender to palpation. The pulp of the affected tooth is nonvital (i.e., it does not respond to thermal changes or to electrical pulp stimulation). In more severe, purulent cases, swelling of the face associated with cellulitis is sometimes present and can be associated with fever and malaise. The affected tooth may be extruded and mobile, both vertically and horizontally. Usually, when facial swelling appears, pain diminishes in intensity, probably owing to rupture of the local periosteum and the decrease in tissue pressure caused by pus accumulation. The diagnosis of these advanced cases is referred to as dentoalveolar abscess. Radiographs are of limited use in the diagnosis of acute periapical periodontitis because no periapical radiographic changes are detected in the early stages. There is a lack of correlation between the periapical radiographic picture, the tooth symptomatology, and the microbiology or histology of the periapical lesion.

Whereas inflammation and pain originate from the periodontal periapical tissues, the source of infection usually lies within the pulp chamber and canal. In order to eliminate this source, the pulp chamber is opened and the root canal de´brided and dressed in accordance with current endodontic practice. Patients with localized periapical pain or swelling generally recover quickly with local treatment, and there is no demonstrable benefit from antibiotic supplementation. Apical abscess should be drained via the tooth or soft tissue incision, and antibiotics are usually of no additional benefit. If cellulitis, fever, and malaise are present, or the medical status of the patient requires this, systemic administration of antibiotics should be instigated.

Lateral Periodontal Abscess Pain characteristics of a lateral periodontal abscess are very similar to those of acute periapical periodontitis and usually result from a blockage of a deep periodontal pocket. Acute periodontal abscesses may also be associated with dental implants. During examination, tender swelling and redness of the gingivae may be noticed, generally more coronally than in acute periapical lesions. The affected tooth is sensitive to percussion and may be mobile and slightly extruded. In more severe cases, cellulitis, fever, and malaise may occur. A deep periodontal pocket is generally located around the tooth and may exude pus. Acute lateral periodontal abscess causes rapid alveolar bone destruction, so a deep infrabony pocket is usually present on the radiograph. Irrigation and curettage of the pocket should be performed. A vertical incision for drainage is recommended when the abscess is fluctuant and cannot be adequately approached through the pocket. When cellulitis, fever, and malaise are present, systemic antibiotic administration may be recommended.

Primary Location

Diagnosis

Pain Intensity

Referral

Clinical Symptoms

Examination Findings

Imaging

Treatment

ANUG

Moderate to severe

Localized

When severe, may spread to the face

Ulcerated interdental papilla, with destruction Fetid odor Painful lymphadenopathy

Not needed

If possible, antiseptic irrigation and local de´bridement Antibiotic therapy

PHGS

Moderate

Diffuse throughout the mouth

Lymph nodes may become very painful

Erythematous gingivae, vesicles or ulceration Lymphadenopathy

Not needed

Hydration, infection control, reduction of fever May need antiviral therapy

Food impaction

Moderate to severe

Localized to affected quadrant

When severe, may spread to the face

Pain around gingivae; worse on brushing and associated with bleeding May report ‘‘tooth tightness’’ or a metallic taste Increasingly seen in adults (third decade) Malaise, fever Vesicular eruption in oral mucosa Vesicles may break down and join to form ragged ulcers Pain after chewing Patient may complain of retained food between teeth

Swollen and red interdental gingivae; easily bleed on probing Open contact point between adjacent teeth; may be due to fractured restoration Food debris may be found

Curettage, if possible, and irrigation Reestablishment of anatomic contacts between teeth with adequate restoration

Pericoronitis

Moderate to severe

Diffuse but located toward the back of the mouth

When severe, may spread to the face

May show fractured restoration. If longstanding may be associated with localized periodontal disease and/or interproximal caries May show an impacted third molar Usually not needed for initial diagnosis

ANUG, acute necrotizing ulcerative gingivitis; PHGS, primary herpetic gingivostomatitis.

Spontaneous pain but may be aggravated by chewing or swallowing

Usually associated with impacted, partially erupted third molars that are partially covered by inflamed gingival tissue Limited mouth opening may be present

Initially, drainage and irrigation may be needed Antibiotics in selected cases If molar impacted, extraction may be needed

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Table 17^4. Current Diagnosis and Therapy of Gingival/Mucosal Pain

V CHRONIC PAIN: NONCANCER PAIN 125

As in periapical periodontitis, the need for antibiotic supplementation, in addition to local treatment, is unclear. Pain generally subsides within 24 hours of treatment.

strictly by b-lactamase–producing anaerobic microorganisms, and the first-line treatment suggested is amoxicillin with clavulanic acid (875 mg twice daily).

Interrelationships between Pulpal and Periodontal Diseases: ‘‘Perio-Endo’’ Lesions

Acute Necrotizing Ulcerative Gingivitis

Deep periodontal pockets can sometimes involve accessory canals (in the furcation or laterally) and, in extensive lesions, can reach the root apex of the tooth and cause retrograde pulp inflammation. A second possibility is of an apical abscess that exudates through a periodontal pocket. Treatment for all these situations is initially endodontic, followed by conventional periodontal treatment. The prognosis of endodontic lesions causing periodontal symptomatology is better than in periodontally initiated lesions.

Vertical Root Fracture A fracture of the tooth that involves most of the root will induce pain on biting. Root fractures are more common in endodontically treated teeth that have been restored with a post and core. The fracture induces a periodontal pocket along its length and may also cause abscess formation. Currently, extraction is the only treatment option for vertical root fractures.

Gingival Pain (see Table 17–4) Food Impaction Food impaction results from food forced between teeth that causes pressure and inflammation of the gums. Localized pain develops between two teeth, usually after meals and especially when food is Ebrous (e.g., meat, celery). The pain is associated with a feeling of pressure and discomfort but may sometimes become severe and diffuse. The patient may report that pain gradually diminishes until evoked again at the next meal or the pain may be relieved immediately by removing the food impacted between the teeth with a toothpick or dental floss. Upon examination, there may be a faulty contact between two adjacent teeth so that food is frequently trapped between these teeth; the gingival papilla is tender to touch and bleeds easily. The two adjacent teeth are usually sensitive to percussion. Prompt treatment is essential to prevent cervical caries and interdental alveolar bone resorption. The cause of the faulty contact between the teeth is often a carious lesion, and restoring the tooth will eliminate the pain. Faulty restorations may also lead to food impaction. In some cases, although the contacts are tight, food impaction may occur, and creating anatomic escape grooves adjacent to the marginal ridge may eliminate food impaction.

Pericoronitis Pain, which may be severe, is generally located at the distal end of the arch of teeth in the lower jaw. Pain is spontaneous and exacerbated by closing the mouth. In more severe cases, pain is aggravated by swallowing, and limited mouth opening may occur. Acute pericoronal infections are common in teeth that are incompletely erupted and partially covered by a flap or operculum of gingival tissue. The operculum is acutely inflamed (red, edematous), and frequently, an indentation of the opposing tooth can be seen on the swollen gingival flap. Occasionally, fever and malaise are present. Irrigation between the operculum and the affected tooth with saline or antibacterial agent will remove debris. Trauma can be eliminated by grinding or extracting the opposing tooth. Systemic antibiotic administration is initiated when there is limited mouth opening or the patient is febrile or immunosuppressed. The infection in pericoronitis is multimicrobial, predominantly caused

Acute necrotizing ulcerative gingivitis (ANUG) is an ulcerative gingival disease characterized by pain, bleeding, and papillary necrosis. Soreness and pain are characteristically felt at the margin of the gums. Pain is intensiEed by eating and toothbrushing; these activities are usually accompanied by gingival bleeding. In the early stages, some patients may complain of a feeling of tightness around the teeth. A metallic taste is sometimes experienced, and generally, there is a fetid odor from the mouth. Pain is localized to the affected areas, but in cases with widespread lesions, pain is experienced throughout mouth. Low-grade fever and malaise are sometimes present, and a regional lymphadenopathy is typical. Necrosis and ulceration are present on the marginal gingiva with different degrees of gingival papillary destruction. Fusiform bacillus and spirochetes are often isolated from gingival ulcers, and ANUG patients often demonstrate an anaerobic flora. An adherent grayish slough represents the so-called pseudomembrane that is present in the acute stage. Acute herpetic infection of the gums (herpetic gingivostomatitis) can sometimes resemble ANUG, but the clinical appearance and associated signs and symptoms are different. The papillary necrosis typical for ANUG is absent in the herpetic infection, whereas herpetic lesions create a typically ‘‘punched-out’’ appearance located at the gingival margin. Treatment includes swabbing and gentle irrigation of the ulcerative lesions, preferably with chlorhexidine or an oxidizing agent (hydrogen peroxide), and scaling and cleaning the teeth. Systemic antibiotics are recommended, especially when fever and malaise are present (amoxicillin/clavulanic acid 875 mg twice daily, metronidazole 250 mg three times daily).

MUCOSAL PAIN Pain originating from the oral mucosa can be either localized or of a more generalized diffuse nature. Localized pain is usually associated with a detectable erosive or ulcerative lesion, whereas diffuse pain may be associated with a widespread infection, a systemic disease, or other unknown factors. The localized pain associated with a detectable lesion results from physical, chemical, or thermal trauma, viral infection, or lesions of unknown origin. Pain is usually mild to moderate, but when there is irritation, mechanically or by sour, spicy, or hot foods, it may become quite severe and last for some minutes. Detailed descriptions of the various lesions of the oral mucosa are beyond the scope of this chapter and only the most common lesions, recurrent aphthous stomatitis, and acute herpetic gingivostomatitis are briefly discussed.

Aphthous Lesions Recurrent aphthous ulcers represent a very common but poorly understood mucosal disorder. They occur in men and women of all ages, races, and geographic regions. It is estimated that at least one in five individuals has at least once been afflicted with aphthous ulcers.2 The condition is classified as minor, major, and herpetiform on the basis of ulcer size and number. Recurrent aphthous stomatitis is characterized by a prodromal burning sensation from 2 to 48 hours before an ulcer appears. Although small in diameter (0.3–1.0 cm), this lesion may be quite painful and induces a painful regional lymphadenopathy. In the mild form, healing occurs within 10 days and pain is usually mild to moderate in severity. In the more severe forms (major

126 Chapter 17  OROFACIAL PAIN aphthous ulcers), deep ulcers occur that may be confluent, are extremely painful, and interfere with speech and eating. Such lesions may last for months, heal slowly, and leave scars. Treatment is mostly symptomatic, including the application of a topical protective emollient for the mild form and the use of topical corticosteroids and tetracycline to decrease healing time for the more severe form. Recently, cyanoacrylate has been used as an effective tissue adhesive for steroids and tetracycline. The use of diclofenac, a topical nonsteroidal anti-inflammatory drug (NSAID), was also found effective.

Acute Herpetic Gingivostomatitis Oral infections caused by herpes simplex type 1 are widespread, even among otherwise healthy people. Whereas most of these herpetic infections are mildly symptomatic, young children are at risk for developing extensive oropharyngeal vesicular eruptions when first infected with the virus. This initial outbreak is known as primary herpetic gingivostomatitis. There has been a general trend for the mean age of patients with acute herpetic stomatitis to increase, and currently the majority of cases (>50%) suffer the first attack during their third decade.3 The incidence of oral herpes simplex infection is particularly high in immunocompromised patients and occurs in up to 50% of hospitalized patients with acute leukemia. Proper diagnosis and treatment are essential, particularly in elderly and immunocompromised patients. The appearance of oral lesions is preceded by a prodromal phase (1–2 days) during which the patient feels unwell and may have fever. Fever, lymphadenopathy, and difficulty eating and drinking are prominent during the active phase. Intraoral vesicles rarely remain intact and rapidly rupture to form ulcers that may coalesce. The gingivae usually appear red and swollen, particularly at the margins. In immunocompetent patients, fever usually recedes within 4 days and the lesions disappear with 10 to 14 days. Although a self-limiting disease, intraoral symptoms may persist for up to 4 weeks, causing significant discomfort. Clinical diagnosis is usually sufficient but may confirmed by laboratory tests. Young children, immunocompromised patients, or adults unable to ingest fluids may require hospitalization to maintain fluid balance, prevent dehydration, control the infection, and provide pain control. A soft, bland diet preceded by a local anesthetic mouth rinse is recommended. Oral hygiene may be maintained by rinsing with a mild bicarbonate or saline solution or a nonalcoholic solution of 0.2% chlorhexidine. Antiviral agents such as acyclovir and famciclovir should be considered part of early management of primary herpetic gingivostomatitis. Providing supportive care and educating parents about transmission of the virus are important.

Diffuse Mucosal Pain When generalized diffuse pain is felt in the oral mucosa, it usually has a burning nature and may be accompanied by a dysgeusia, predominantly of a bitter metallic quality. This pain may result from a direct insult to the tissues due to bacterial, viral, or fungal infection, which can be identiEed by the characteristic appearance of the oral mucosa. Diagnosis is aided by microbiologic and other laboratory examinations. In cases of chronic fungal infection (candidiasis), possible underlying etiologic factors such as prolonged broad-spectrum antibiotic therapy, immunodeEciencies, and other debilitating factors should be investigated. Radiation therapy to the head and neck region may result in acute mucositis with severe generalized mucosal pain. Decreased salivary flow is a late sequela of radiation therapy that may result in chronic pain and discomfort of the oral mucosa. Burning sensation of the oral mucosa, particularly the tongue, may result from systemic diseases, such as chronic iron deEciency anemia, and may be associated with

atrophic glossitis. This is usually associated with observable atrophic changes of the tongue, in particular absence of Eliform and fungiform papillae. Atrophic glossitis and burning mouth sensations have also been associated with Helicobacter pylori colonization of tongue mucosa and nutritional deficiency.

PAIN FROM SALIVARYGLANDS Pain from the salivary glands is usually associated with salivary gland duct blockage. Pain from salivary glands is localized to the affected gland and is of moderate to severe intensity. The salivary gland is swollen and very tender to palpation. Salivary flow from affected glands is reduced and sometimes completely abolished. Pain is intensified by increased saliva production, such as when starting meals, and can be induced by applying an acidic stimulant (citric acid is the standard stimulant) to the tongue. Many cases of salivary gland blockage are associated with ascending bacterial infection of the gland. Pus may be secreted from the salivary duct when the gland is infected, and pain may be associated with fever and malaise. When blockage is diagnosed, surgical or endoscopic approaches are indicated to remove the blockage. In the acute bacterial infection stage, antibiotic therapy is recommended. No antibiotics are recommended for mumps or recurrent parotitis.

TEMPOROMANDIBULAR DISORDERS Temporomandibular disorder (TMD) is an umbrella classification that includes ailments of the temporomandibular joints (TMJs) and masticatory muscles. TMD-related facial pain has been found to occur in 4% to 12% of the population, and severe symptoms are reported by 10% of subjects. Some signs or symptoms of TMD are extremely common, joint clicking, for example, is found in 20% to 30% of the population. However, only 3% to 11% are assessed as needing treatment. These figures are compatible with the data on the percentage of individuals who seek treatment (1.4%–7%). Masticatory muscle and TMJ tenderness were found in 15% and 5%, respectively, of a large population examined.4 However, muscular tenderness was self-reported by only about a third of these, suggesting that many patients have asymptomatic muscle tenderness. Signs and symptoms of TMD have been found in all age groups, peaking in 20- to 40-year-olds. Signs of TMD have been described in children and adolescents but are usually mild. In a group of adolescents, treatment need was assessed at 7%.5 TMDs may also occur in edentulous patients. Accumulated evidence suggests that symptoms in the elderly may be lower than in the general population, but some studies show a slight elevation in the prevalence of some signs (e.g., joint sounds, limited mouth opening) in this age group.6 There is a female preponderance of TMD signs and symptoms, especially of muscular origin. Most studies also report that the vast majority of patients (up to 80%) who seek treatment are females7 (Tables 17–5 and 17–6).

Masticatory Myofascial Pain The diagnosis of masticatory myofascial pain (MMP) is based on the history and clinical examination of the patient. MMP is characterized by regional, unilateral pain around the ear, the angle/body of the mandible, and the temporal region (see Table 17–5). Referral patterns include intraoral, auriculotemporal, supraorbital, and maxillary areas, depending on the muscles involved and the intensity of the pain. Pain is aggravated during jaw function, with transient spikes of pain occurring spontaneously. In addition to pain, there may be deviation of the mandible on opening, fullness of the ear, dizziness, and soreness of the neck, particularly if muscle trigger

Table 17^5. Current Diagnosis of Temporomandibular Disorders Diagnosis

Pain Intensity

Primary Location

MMP

Moderate

Angle of mandible, Depending on temporal, involved muscles: periauricular forehead, neck, and intraoral regions

Referral

ADDwR

Moderate to severe

Periauricular

Ear, angle of mandible

ADDwoR

Moderate to severe

Periauricular

Ear, angle of mandible

DJD

Moderate to severe

Periauricular

Ear, angle of mandible Muscles of mastication Headache, neck pain

IJD

Moderate to severe

Periauricular

Ear, angle of mandible Headache, neck pain

Clinical Symptoms

Examination Findings

Imaging

Not relevant

MRI or arthrography: displaced articular meniscus (reducing)

MRI or arthrography: displaced articular menisus (non-reducing) Plain radiographs or CT: may be degenerative changes with microcystes, hypercortication and osteophyte formation

Destruction of articular surfaces Often similar radiographic picture as in DJD

ADDwR, anterior disk displacement with reduction; ADDwoR, anterior disk displacement without reduction; CT, computed tomography; DJD, degenerative joint disease; IJD, inflammatory joint disease; MMP, masticatory myofascial pain; MRI, magnetic resonance imaging; TM, temporomandibular; TMJ, temporomandibular joint.

V CHRONIC PAIN: NONCANCER PAIN 127

Tender pericranial, masticatory and cervical muscles Myofascial trigger points Deviation and limitation of mouth opening Ethyl chloride spray onto muscle relieves pain and increases mouth opening Pain on chewing Tender TM joint, associated with reciprocal Joint sounds clicking Deviation to affected side on mouth opening May have pain on loading the joint by biting a hard stick contralaterally Pain on chewing Very tender TM joint. Deviation to affected May report a history of joint side and limitation of mouth opening. Pain sounds on loading the joint by biting a hard stick Unable to fully open mouth contralaterally. Very tender TMJ; may occur bilaterally Pain and difficulty with Usually associated with crepitation in the chewing affected joint Stiffness of the jaws; usually There may be no initial correlation between worse in the evening but clinical and imaging findings not particularly severe in Pain on loading the joint by biting a hard the morning (if so, lasts stick contralaterally. < 30 min) Very tender, often swollen, TMJ Pain and difficulty with Usually associated with crepitation in the chewing affected joint Stiffness of the jaws and May occur bilaterally pain in the muscles TMJ involvement usually occurs in advanced Jaw stiffness is particularly stages of generalized inflammatory severe in the morning and arthritides lasts > 30 min Joint destruction may lead to an anterior open bite Depending on underlying disorder associated with autoimmune or hematologic abnormalities Continuous pain, exacerbated on chewing Difficulty in chewing Acute malocclusion: clinically unverifiable

128 Chapter 17  OROFACIAL PAIN

Table 17^6. Current Therapy of Temporomandibular Disorders Diagnosis

Treatment Options

MMP

Physical: Home or institutional physiotherapy to maintain muscle strength and mobility and restore normal mouth opening. Spray (with ethyl chloride) and stretch exercises. Biofeedback, soft laser, physical self-regulation program (breathing training, postural relaxation, and proprioceptive reeducation). Soft diet: For acute cases, a soft diet allows the muscles to rest. Bite appliance: Flat occlusal appliance made of hard acrylic. Adjusted intraorally to maintain even contacts. Usually worn only during sleep. Pharmacologic: Acute cases may be treated with analgesics or NSAIDs: Paracetamol/acetaminophen 250–500 mg qid; naproxen 500 mg bid; ibuprofen 200–400 mg qid. Chronic cases may require tricyclic antidepressants: amitriptyline (10–35 mg daily), cyclobenzaprine (10–30 mg/day), clonazepam (0.5 mg daily), or gabapentin (2700–3600 mg daily). Psychological: Cognitive behavioral therapy. Trigger point injection: Lidocaine (2%), mepivacaine (3%), or procaine injection into muscle trigger points. Physical: As above. Bite appliance: Repositioning appliances have been advocated to recapture the disk; however, they fail to do so in the long term, so we suggest flat appliances as above. Some data suggest that contacts on the posterior region of the bite plate may lead to off-loading of the joint and may be used initially. Readjustment of the plate to allow full contacts should be performed to prevent occlusal changes. Pharmacologic: NSAIDs are usually required to reduce symptoms. Comorbid MMP should be treated concomitantly, as above. Arthrocentesis: Is able to restore mouth opening in disk displacement without reduction and may improve symptoms in other intra-articular disorders. Surgery: Either arthroscopic or open is reserved for resistant cases or cases with other clear indications for surgery (hyperplasia, ankylosis).

TMJ pain

MMP, masticatory myofascial pain; NSAIDs, nonsteroidal anti-inflammatory drugs; TMJ, temporomandibular joint.

points are present. Pain is dull, heavy, tender, and rarely, throbbing, and the severity may fluctuate during the day but is moderate; the average pain duration is about 5.5 hours. Some patients experience the most intense pain in the morning (21%) or late afternoon (79%), and others have no fixed pattern. Pain-free days may be reported, and fortunately, the pain rarely wakes the patient. MMP has been clearly shown to be a chronic or fluctuating pain condition; over 5 years, 31% of patients suffered continuous MMP, 36% experienced recurrent pain, and 33% remitted.8 Examination usually reveals limited active mouth opening (<40 mm, interincisal). Forced (passive) opening by the examiner may reveal a slightly increased opening. Tenderness to palpation is usually present in masticatory muscles unilaterally, and it is a distinguishing feature of MMP patients. The masseter is the muscle most commonly involved (>60%), the medial pterygoid and temporalis muscles are tender in about 40% to 50% of cases, commonly unilaterally. The sternocleidomastoid, trapezius, and suboccipital muscles are usually tender in 30% to 45% of patients, very often bilaterally. Typically, there are localized tender sites and trigger points in muscle, tendon, or fascia. A hypersensitive bundle or nodule of muscle fiber of harder than normal consistency is the physical finding most often associated with a trigger point. Trigger points may be associated with a twitch response when stimulated. In addition, trigger point palpation may also provoke a characteristic pattern of regional referred pain and/or autonomic symptoms. Referral to the teeth may be prominent and may often cause misdiagnosis as dental pathology.

Pain Associated with theTMJ The most common conditions associated with pain of the TMJ are internal derangements, which may be painful when associated with joint inflammation (Fig. 17–1 and Table 17–5). More rarely, degenerative joint disease (DJD) or inflammatory arthritic diseases may affect the TMJ. Often, these TMJ entities are comorbid with muscle pain, usually MMP, and thus require a combined treatment

approach. More rarely, the TMJ may be affected by infectious or metabolic arthritides which are not be dealt with in this chapter. Internal derangement signifies an abnormal anatomic relation between the condylar head and the articular disk when the teeth are in normal occlusion. In most cases, the disk is anteriorly displaced (see Fig. 17–1B).

AnteriorDiskDisplacementwithReduction (see Fig. 17–1B and C) During mouth opening, the condyle on the affected side meets the posterior band of the anteriorly displaced disk, encounters some resistance, then moves under the disk proper (reduction). During closing, the condyle will slip off the anteriorly positioned disk and return into the glenoid fossa. The sound that the condyle makes on mounting the disk during opening and then slipping off during closing causes the characteristic reciprocal clicking of anterior disk displacement with reduction (ADDwR). Patients with ADDwR may be totally asymptomatic and report only joint clicking or popping sounds that may or may not bother them. ADDwR may, however, be symptomatic with pain that is associated with chewing, particularly hard foods. The affected TMJ may be tender to palpation. Although pain is usually mild, it may become moderate to severe with VAS scores of 6 to 7. When the disk is displaced unilaterally, the mandible will deviate to the affected side during opening until the first click occurs—this signifies ‘‘reduction’’ or a return to normal relationship. Mouth opening then continues undeviated and is usually not limited; there may be some pain at maximal opening.

Anterior Disk Displacement without Reduction (see Fig. 17–1C and D) In anterior disk displacement without reduction (ADDwoR), the condyle is unable to mechanically pass under the disk, and therefore, there is no reduction. Attempts to open the mouth further induce pain located over the joint and are usually associated with no increased opening. The joint is generally very tender to palpation.

V CHRONIC PAIN: NONCANCER PAIN 129

Closed

Maximal Opening

4 2 normal

wR

A

1

AD D

3

B

Radiographic evidence of DJD is very common (14%–44%) in asymptomatic individuals, but only 8% to 16% will have clinically detectable disease. DJD affects women, particularly after the age of 40 to 50. Pain is located in the TMJ and periauricularly and may spread to adjacent structures. Patients complain of difficulty in chewing, jaw stiffness, and tiredness. Jaw stiffness is usually more severe in the evening. The TMJ and muscles of mastication are very tender. Mouth opening is restricted and deviates to the affected side; crepitation is generally present. Imaging often reveals subchondral bone sclerosis, flattening, lipping (osteophyte formation), and microcyst formation. DJD may occur after trauma to the TMJ and may be more severe in its clinical presentation than its primary counterpart.

Inflammatory Joint Disease

ADDwoR

C

D

Figure 17^1. Internal derangements of the temporomandibular

joint. A, Normally when the mouth is in the closed position, the condyle lies below the articular disk.B, Mouth opening begins with rotational movement followed by translation of the condyle over the eminence to the maximal opening, which is usually 40 mm or more; movementis fully coordinated with the disk.C, In ADDwR, the disk is anteriorly located relative to normal, often the condyle is located under the posterior attachment.During opening, the condyle reduces (resumes a normal position) under the disk and full opening is unlimited and characterized by a normal condyle/disk relation.D, In ADDwoR, the disk is anteriorly located relative to normal but is unable to reduce during opening; mouth opening remains limited and the disk remains anteriorly displaced, even at maximal opening (usually < 30mm). Movement is thus on the posterior attachment.1, condyle; 2, articular disk, 3, posterior attachment; 4, fossa; 5, eminence; ADDwoR, anterior disk displacement withoutreduction; ADDwR, anterior disk displacement with reduction.

Analysis of fluids obtained from the upper joint space during arthrocentesis reveals proinflammatory cytokines so that an active inflammatory process is present. Pain in ADDwoR may become quite severe with VAS scores of 7 to 9 and will severely affect the patient’s functional capabilities. The patient will present with limited mouth opening (20–25 mm) and a sharp deviation to the affected side when asked to open the mouth. Onset is usually acute and may be preceded by a history of ADDwR. In some patients, there may be a slow transition from ADDwR to ADDwoR. The patient has a consistent reciprocal click but reports that, at times, sudden-onset restricted mouth opening occurs with no click. Mandibular movements often relieve this situation, and the patient returns to ADDwR; this condition is simply termed ADDwR with intermittent locking. If ADDwoR is untreated, a degree of physiologic adaptation occurs whereby the articular tissues are stretched and the patient may therefore present with minimally limited mouth opening (30–35 mm) accompanied by a lesser degree of deviation.

DJD DJD is a chronic noninflammatory disease that affects the articular cartilages of synovial joints, particularly load-bearing ones.

The TMJ may be involved in the clinical presentation of a number of systemic arthritides including rheumatoid and psoriatic arthritis. In most cases, the patient is already diagnosed, and TMJ involvement is a sign of increasing disease severity. The management of such cases, therefore, involves the addition of selected TMD-specific therapies to the existing treatment. The TMJ may be very painful, at times swollen, and will limit function. Imaging reveals joint destruction similar to that observed in DJD but often more rapid in its progression. Laboratory findings may include a raised erythrocyte sedimentation rate, anemia, leukocytosis, and the presence of autoantibodies.

Treatment Not all patients with acute TMDs will develop a chronic pain disorder. Predictors of chronicity include high initial pain intensity, high disability score, higher scores of emotional distress, the presence of myofascial pain (versus TMJ disorders), and female gender. Patients developing chronicity also differ significantly in numerous biopsychosocial variables (e.g., they suffer from more current anxiety disorders, mood disorders, and somatization disorders). Treatment of TMDs with a variety of conservative methods consistently results in high (75%–90%) success rates. In general, treatment is aimed at palliation and is based on clinical diagnosis; because the etiology is unclear, no treatment is curative. Extensive research shows that there are no compelling data to support any intervention as capable of TMD eradication or modification. Moreover, conservative therapies are consistently successful and in no way inferior to more invasive or irreversible procedures such as surgery, occlusal adjustment, and prosthetic rehabilitation. The data thus support a conservative approach to the management of TMDs. This is reinforced by findings that the natural history of TMD includes an extensive number of patients who will either substantially fluctuate or remit over time and rarely progress to severe pain. Treatment aims in TMD patients include reducing pain, restoring function and range of motion, decreasing or eliminating aggravating or contributing factors, and increasing bite comfort and muscle strength. In addition, we aim to reduce psychological distress, restore social functioning, and cease or prevent drug abuse. The assessment of treatment outcome is based on accurate assessment of pain intensity and frequency and the evaluation of changes in psychosocial comorbidity. Therapy for TMDs falls into a number of categories: physical, pharmacologic, psychological, trigger point injection (for MMP), TMJ arthrocentesis, or TMJ surgery and is often multidisciplinary. Treatment of TMD very often combines conservative interventions, and different centers have variable protocols depending on patients’ signs and symptoms and clinician’s preferences. Treatment duration is generally 4 to 6 months but may be longer in selected cases (see Table 17–6).

130 Chapter 17  OROFACIAL PAIN

Physical and Combined Modalities Most pain physicians with experience in the field of TMD will attest to the success of conservative physical therapy, including muscle exercise, thermal packs, and oral splints. However, few, if any, of these therapies have been subjected to controlled trials. Often, reassurance and education of the patient combined with simple exercises for the TMJ, masticatory, and neck muscles will result in pain alleviation and restored mandibular function. Muscle tenderness may be also treated with vapocoolant sprays and concomitant stretching—‘‘spray and stretch.’’ This usually induces immediate relief and is often employed as a diagnostic test. Other commonly used techniques such as ultrasound and thermal packs have also not been rigorously assessed. Transcutaneous electrical nerve stimulation (TENS), low-level laser, and physical self-regulation (PSR) programs are sometimes effective in TMDs. Many studies indicate the importance of education and self-care in the management of TMDs.9

Occlusal Splints Flat occlusal splints (relaxation or stabilizing splints) are in widespread use and provide even occlusal contacts; these may be constructed for the upper or lower jaw. There seems to be no difference in effect between flat splints, anterior midline stop devices, and canine guidance splints. We do not recommend partial coverage splints owing to the inherent potential to cause permanent occlusal changes and the lack of evidence for any advantage over flat splints. Meta-analyses consistently demonstrate benefit for oral splints in TMDs in general: both TMJ arthralgia and MMP.10 The presence of widespread pain reduces the effectiveness of oral splints and suggests that these should be prescribed for patients with regional myofascial face pain only. The number needed to treat (NNT) for occlusal appliances in the treatment of TMDs has been calculated: an NNT of 6 for TMJ pain and 4.3 for MMP.10 The relatively good success rate and highly conservative nature of splints account for their extensive use. They do, however, entail higher costs than other therapies.

Pharmacologic NSAIDs are used extensively in the management of pain and disability associated with joint disease. Selective cyclooxygenase (COX)-2 inhibitors and some of the older nonselective COX inhibitors have potentially serious side effects on the renal and cardiovascular system, and long-term therapy is contraindicated. For the treatment of TMDs, calculations of NNTs for drugs versus placebo reveal encouraging figures of 2.7 to 3.5. Ibuprofen (400 mg three times daily) and naproxen (500 mg twice daily) are good choices. In patients with gastrointestinal discomfort, we recommend the addition of antacids (e.g., proton pump inhibitor; omeprazpole). Simple analgesics or combination analgesics (e.g., codeine and paracetamol/acetaminophen) may also provide good analgesia and may be safer than NSAIDs. Amitriptyline at low doses (10–30 mg/day) provides consistent benefit for patients with craniofacial myofascial pain, including predominantly muscular TMDs, and post-traumatic myofascial pain. Clonazepam (0.5 mg daily), a long-acting benzodiazepine with anticonvulsant properties, or cyclobenzaprine (10–30 mg daily), a muscle relaxant, is beneficial in predominantly muscular TMDs. Gabapentin (2700–3400 mg daily) is effective for the treatment of MMP with an NNT of 3.4.11

Biobehavioral Therapy Pain is a subjective experience with important affective, cognitive, behavioral, and sensory components. Outcomes including restoration of functional activity, eradication of drug abuse and dependency, and rehabilitation of residual emotional distress need to be

addressed. The assessment of psychological distress in MMP patients may be performed with established questionnaires. Cognitive-behavioral therapy (CBT) is an option that aims at altering negative overt behavior, thoughts, or feelings in chronic pain patients and to diminish distress and suffering. Whether separately or combined with other pain treatments, CBT produced significantly decreased pain, emotional distress, and disability and is of proven efficacy in TMD patients.12 Biofeedback aims to teach the patient to control behavior that is possibly part of the pain etiology and is efficacious in regulating muscle tension in TMD patients with good long-term results. Combination of biofeedback with CBT techniques significantly improves treatment outcomes versus CBT alone.

Trigger Point Injections and Needling Injections of local anesthetics into trigger points induce pain relief that may be prolonged beyond the effect of the anesthetic agent. The technique for the head and neck muscles is simple and involves the location and immobilization of the trigger point followed by injection using a standard technique. In myofascial pain patients, bupivicaine (0.5%) is equiefficacious to botulinum toxin in the relief of pain, and cost-effectiveness would suggest the former’s preferential use. We initially use mepivacaine (3%) to test patient response. If the results are encouraging and the patient needs further injections, we may then employ bupivacaine (0.5%), although there are reports of bupivicaine-induced damage to muscle fibers. Based on an extensive literature review, direct (or ‘‘dry’’) needling of myofascial trigger points appears to be an effective treatment, most likely because of the needle or placebo rather than the injection of either saline or active drug. Dry needling of trigger points is very similar to some acupuncture techniques.

Arthrocentesis Arthrocentesis, or lavage, of the upper TMJ space is a very simple technique that involves the introduction of two large-bore hypodermic needles into the superior joint space and rinsing with 400 to 600 ml of sterile saline or lactated Ringer’s. This volume is the minimum needed to eliminate proinflammatory cytokines that have accumulated in the joint space. Arthrocentesis is commonly used to treat ADDwoR, particularly of sudden onset, but may also be employed to palliate pain in ADDwR, degenerative, or inflammatory TMJ disease.

Surgery TMJ surgery may be performed with an arthroscope or via an open approach. In general, TMJ surgery is reserved for medically recalcitrant cases and is rarely employed for the control of TMJ pain.

Complementary and AlternativeTherapy Approximately 20% of facial pain patients in a referral center had attended a complementary and alternative medicine (CAM) specialist previously, and up to 36% of TMD patients reported treating their symptoms with CAM techniques. The existing evidence supports the value of acupuncture for the management of idiopathic headaches and has shown promise in the management of TMDs. However, well-planned studies are needed to assess the clinical value and cost-effectiveness of acupuncture and other CAM therapies for facial pain.

FACIAL MIGRAINE, NEUROVASCULAR OROFACIAL PAIN (Tables 17–7 and 17–8) Aberrant migraine locations are not recognized by the International Headache Society (HIS) or the International Association for the

Table 17^7. Current Diagnosis of Neurovascular Orofacial Pain (NVOP)

Diagnosis

Pain Intensity

Facial Moderate migraine/NVOP to severe

Severe

Paroxysmal hemicrania (PH){

Severe

SUNCT{

Severe

Hemicrania continua{

Moderate

Intraorally. Middle and lower third of the face

These entities are usually associated with a primarily periorbital location

Infraorbitally, periauricular

Commonly to temporal, frontal and cervical regions. Very commonly to intraoral regions

Upper 2/3 of the face and intraorally

Examination Findings

Imaging

Also pressing pain that may wake from sleep.

+++

Also neuralgic. Occurs in cluster or chronic. Lasts 15–180 minutes and may occur up to 8/day.* Restlessness More frequent (8–30/ Thorough examination to Chronic PH is often day) than CH but exclude dental pathology. associated with shorter lasting (2–30 Often mild pericranial/ systemic disease. min).* masticatory muscle tenderness is present. Cranial nerve examination should be performed to identify symptomatic cases. Sharp, stabbing lasts Most common mimics 2–240 seconds. of SUNCT are lesions Extremely high in the posterior fossa frequency (2–200/ or involving the day). May have pituitary gland. trigger areas similar to trigeminal neuralgia Continuous unremitting. Exacerbations resemble migraine

++

++

Temporal, frontal, periorbital

Clinical Symptoms

+/

+

*In addition to the episodic form, a chronic form exists. { See Section V, Chapter 16, Headaches Other than Migraine. SUNCT, short-lasting neuralgiform headache attacks with conjunctival injection and tearing. Patients with atypical findings or symptomatology may require brain imaging to exclude pathology.

Important to exclude dental pathology or sinusitis. In selected cases, brain imaging to exclude pathology Up to 4% of patients with pituitary tumors have CH.

V CHRONIC PAIN: NONCANCER PAIN 131

Cluster headache (CH){

Primary Location Referral

Clinical Features: Usually Throbbing. Variable autonomic activation

132 Chapter 17  OROFACIAL PAIN

Table 17^8. Current Therapy of Neurovascular Orofacial Pain Diagnosis

Treatment

Facial migraine/ NVOP*

Abortive{: Naproxen sodium (825 mg stat) Triptan therapy: No specific evidence base for facial migraine/NVOP but works in selected cases Prophylactic{: b-Blockers (propranolol SR 80–160 mg/day), antiepileptic drugs (divalproex SR 500 mg/day), tricyclic antidepressants (amitriptyline 10–50 mg/day) Abortive{: Sumatriptan, dihydroergotamine, oxygen Prophylactic: Verapamil, AEDs, prednisone, lithium§ Indomethacin{

Cluster headache*{

Paroxysmal hemicrania*{ SUNCT{ Hemicrania continua{

Lamotrigine (currently considered drug of choice), gabapentin, topiramate Indomethacin

*Episodic and chronic forms that will dictate approach to therapy. { See Section V, Chapter 16, Headaches Other than Migraine. { See Section V, Chapter 16, Headaches Other than Migraine. § Effective for chronic cluster headache. AED, antiepileptic drugs; NVOP, neurovascular orofacial pain; SR, sustained-release; SUNCT, short-lasting neuralgiform headache attacks with conjunctival injection and tearing.

Study of Pain (IASP). However, many patients present with a primary lower facial pain characterized by classic neurovascular features, including autonomic signs, nausea, and photo- or phonophobia. These may be termed neurovascular orofacial pain (NVOP), or facial migraine. Theoretically, migraine mechanisms may present in the facial or oral region, and primary orofacial pain of neurovascular origin is of great diagnostic and therapeutic importance. NVOP patients often present with dental symptomatology (thermal hypersensitivity), and the similarities with dental pulpitis have obviously caused diagnostic difficulties.

Clinical Features of Facial Migraine/NVOP The vast majority of patients report unilateral pain. Pain occurs primarily at an intraoral site, usually around the alveolar process, but may be associated with a mucosal site. Referral of pain is evenly divided between perioral structures (e.g., lips, chin), the periorbital region (usually infraorbital), and the periauricular region. Moderate to strong episodic pain characterizes NVOP. In about half the cases, the pain throbs and, in one third, woke the patient from sleep. Pain may last from minutes to hours or, more rarely, continues for more than 24 hours. Many cases are characterized by a chronic highfrequency pattern. Pain can be accompanied by various local autonomic signs such as tearing, nasal congestion, a feeling of swelling or fullness of the cheek, and a complaint of excessive sweating. Other phenomena such as photo- or phonophobia and nausea

are observed. Patients may report dental hypersensitivity to cold, leading to diagnostic confusion. The onset of NVOP is around 35 to 50 years of age, and it affects females more often than males (3–10:1). Time to diagnosis was, on average, 34 to 101 months (range 1–528 mo), attesting to the diagnostic difficulties presented by these patients.13 Often, patients have a positive history of migraine. In 38% to 45% of cases, the pain was diagnosed as secondary to dental pathology, and patients underwent dental treatment with no success. Some cases (36%) underwent repeated extractions in the same quadrant. Low-dose amitriptyline, b-blockers, and ergotamine have been successful in NVOP or facial migraine. No trials with triptans have appeared in the literature. The drugs and guidelines outlined in Section V, Chapter 15, Migraine Headaches, are relevant for NVOP (see Table 17–8).

TRIGEMINAL AUTONOMIC CEPHALGIAS Pain quality in trigeminal autonomic cephalgias (TACs) and dental pulpitis is similar, and dentists are often the first health care providers consulted. Incorrect diagnosis may lead to dental treatment that is both misguided and unjustified. Peak pain intensity in TACs is classically felt periorbitally or in the eye. However, ‘‘lower’’ and ‘‘upper’’ subtypes of cluster headache have been reported; pain in ‘‘lower cluster headache’’ is ocular, temporal, and suboccipital with radiation to the teeth, jaws, and neck and is therefore highly relevant. Intra- or perioral radiation of pain includes the jaws (37%), teeth (maxillary 50%; mandibular 32%). and cheeks (45%).13 In ‘‘upper cluster headache,’’ pain is periorbital but radiates to the forehead and temporal and parietal regions. Referral patterns of TACs often involve orofacial structures and, at times, may primarily present in intraoral or unusual facial sites. Some TACs are characterized by short, repeated, and severe pain that may be pulsatile and similar to the inflammatory symptoms of pulpitis. Thus, patients with cluster headache (35%–45%), paroxysmal hemicrania (15%), and hemicrania continua (rarer) report toothache-like pain, and many will undergo unnecessary dental interventions. Thorough clinical and radiologic dental evaluation usually eliminates a dental cause in these cases. Referral patterns of migraines and cluster headaches include the areas over the paranasal sinuses, and migraine or cluster headache are common diagnoses in otolaryngology settings. Up to 10% of patients with paroxysmal hemicrania have pain triggered by neck movement, causing confusion with musculoskeletal pain syndromes. Some of the cases reported demonstrated ipsilateral masticatory muscle tenderness, and although confusing, this is consistent with findings in other primary neurovascular-type headaches such as migraine, particularly chronic migraine (see Section V, Chapter 15, Migraine Headaches). Hemicrania continua patients may also describe pain that refers to the jaw, ear, and mastoid and could be confused with pain arising from TMDs. However, although hemicrania continua and TMDs are both continuous, TMDs rarely wake the patient from sleep and are not throbbing in character.

NEUROPATHIC OROFACIAL PAIN (Tables 17–9 and 17–10) Neuropathic pain may develop after a number of insults to the peripheral or central nervous systems. Peripheral pain syndromes include traumatic neuropathies, diabetic neuropathy, and postherpetic neuralgia. These peripheral processes are almost invariably complicated by dysfunction of nociceptive pathways in the central nervous system. Central pain may be caused by direct damage as in stroke and spinal cord trauma or after centrally occurring diseases

V CHRONIC PAIN: NONCANCER PAIN 133

Table 17^9. Current Diagnosis of Neuropathic Orofacial Pain* Diagnosis

Pain Intensity

Post-traumatic Mild to severe neuropathy

BMD

Moderate (severe in some)

TN*

Severe

Postherpetic TN{

Moderate to severe

Primary Location

Referral

Clinical Symptoms Examination Findings

Imaging

May be associated with May be associated with skeletal areas of scar tissue fractures or other Affected areas may pathology that demonstrate allodynia, induces nerve dysesthesia, analgesia, damage redness Temporal summation may occur Irrelevant Primary or idiopathic Tongue, lips Localized Idiopathic onset BMD must not be due Very frequently to any local or systemic observed in factor postmenopausal Secondary BMD may women occur in local mucosal Continuous burning sensation disease and a number of metabolic and May be associated endocrine disorders with taste and salivary secretion disturbances Advanced techniques Short (seconds to Usually none Usually Second and may show Quantitative sensory 2–3 min), dermatomal third testing may reveal mild neurovascular paroxysmal pain dermatomes Referral to contact at the CN sensory deficits May be triggered of CN 5 teeth very Focal neurologic findings 5 root TN may also by innocuous common may indicate pathology. occur secondary to stimuli or tumors and Trigger area may be spontaneous multiple sclerosis identified that induces May have background pain pain and subsequently becomes refractory. (atypical TN) or begin in an uncharacteristic fashion pre-TN Usually first Usually Burning, constant Scars, hypopigmented Irrelevant dermatome of localized but pain regions CN 5 may spread if Superimposed Scars may be severe flashes of pain hyposensitive or allodynic

Initially localized, dermatomal

Adjacent structures, may cross midline

Onset associated with traumatic event Burning or lancinating, electrical pain.

*See Section V, Chapter 35, Trigeminal Neuralgia. { See Section V, Chapter 36, Postherpetic Neuralgia. BMD, burning mouth disorder; CN, cranial nerve; TN, trigeminal neuralgia.

such as epilepsy, Parkinson’s disease, and multiple sclerosis (MS). Pain due to MS may resemble TN (see Section V, Chapter 35, Trigeminal Neuralgia).

Central Poststroke Pain Facial pain is common in brainstem lesions, particularly of the lower medulla, and may cause constant burning or paroxysmal sharp pain. About 50% of patients with lateral medullary infarcts suffered ipsilateral facial pain with or without accompanying body pain. Facial pain is located periorbitally and is burning or hot, stinging, and pressure-like. Persistent pain with superimposed attacks occurs in 25% of patients, and 42% have only paroxysmal pain lasting seconds to minutes. Ipsilateral sensory dysfunction and corneal reflexes were not present in all facial pain patients.14 Amitriptyline as well as the anticonvulsant lamotrigine may be

effective in central poststroke pain (CPSP), and these should be considered first. Gabapentin and the sodium channel blocker mexilitene are reasonable second choices. Short-term relief may be obtained with intravenous lignocaine or propofol. Unfortunately, some poststroke patients may not be good medical candidates for tricyclic antidepressants (TCAs), and anticonvulsants are therefore indicated.

TN TN is an excruciating short-lasting, unilateral facial pain with clear classification criteria (see Section V, Chapter 35, Trigeminal Neuralgia). In 16% to 18% of patients, the singly affected nerve in TN will be the maxillary or the mandibular branch, whereas the ophthalmic is affected singly in only about 2% of cases.14 Most commonly, the maxillary and mandibular branches are affected

134 Chapter 17  OROFACIAL PAIN

Table 17^10. Current Therapy of Neuropathic Orofacial Pain* Diagnosis

Treatment Options

Post-traumatic Gabapentin (300 mg/day initial for 3 days; neuropathy increase by 300 mg every 3 days until 300 mg tid. If response is positive, titrate up to 2700 mg/day) Tricyclic antidepressants (amitriptyline 10 mg/ day initially up to 50 mg/day) SNRIs (venlafaxine SR 37.5 mg/day initially up to 150 mg/day) Pregabalin Opioids Combination therapies (gabapentin/venlafaxine; gabapentin/opioids) Topical medications{: 5% lidocaine patches, topical antiepileptic drugs, or tricyclic antidepressants in stents Alpha lipoic acid (600 mg/day) Burning Topical clonazepam (1 mg; ‘‘suck and spit’’ tid) mouth Tricyclic antidepressants disorder TN* Carbamazepine Oxcarbazepine Baclofen Lamotrigine{ Gabapentin. Surgical (best prognosis in typical TN early after onset):  Peripheral level  Ganglion level  Trigeminal root level Postherpetic Topical lidocaine{ TN* Tricyclic antidepressants Gabapentin Opioids *See Section V, Chapter 35, Trigeminal Neuralgia, and Chapter 36, Postherpetic Neuralgia. { Lamotrigine has been proven effective as an add-on therapy. { Topical medications may be unsightly on the face. Intraorally, they require construction of a carrier stent. SNRI, selective serotonin-norepinephrine reuptake inhibitors; SR, sustained-release; TN, trigeminal neuralgia.

together (35%), and all three branches are involved in 14% of patients. The jaws are, therefore, involved in most cases, explaining why TN patients so often seek help from dentists. Pain radiation is generally within the dermatome of origin. TN may mimic dental pain, and a quarter of cases will initially consult a dentist. Unfortunately, TN is often misdiagnosed, and 33% to 65% of cases may undergo unwarranted dental interventions; up to 12% may be eventually rendered edentulous. The numbers of TN cases with extensive and misguided dental interventions suggest a lack of awareness of many dentists to the features of TN. However, TN may occasionally present atypically and resemble dental pathology; in these cases, it is more difficult to diagnose. Thorough clinical and radiographic dental examinations are essential, and invasive dental treatment must not be performed without positive anamnestic, clinical, and radiographic findings.

Unusual TN Presentations Up to 30% of TN patients report atypical features: longer TN pain attacks and a constant background pain. This is diagnostically and therapeutically relevant; microvascular decompression provided absolute postoperative pain relief in typical or classic TN (CTN) for 80% of cases but for only 47% of atypical TN cases. Long-term follow-up (>5 yr) revealed excellent results in 75% of CTN but in only 35% of atypical TN cases.14 An early form of TN termed pretrigeminal neuralgia (PTN) has been described. PTN has been reported in 18% of TN patients and is characterized by a dull continuous pain in one of the jaws that lasts from days to years. As the process continues, PTN becomes more typical with characteristic flashes of pain. Thermal stimuli may cause triggering at a relatively higher rate, and a throbbing quality to PTN pain is sometimes present, mimicking dental pathology. Indeed, these qualities combined with the success of regional anesthesia have led to misdiagnosis of PTN as pain of dental origin. PTN is, however, highly responsive to anticonvulsant therapy. Our clinical experience confirms that there are cases with highly atypical features that respond to carbamazepine and develop into TN. However, the lack of clear and consistent diagnostic criteria makes this a problematic entity to recognize; it is usually diagnosed when all other possibilities are exhausted or in retrospect once CTN develops.

Burning Mouth Disorder Burning mouth disorder (BMD) is a poorly understood pain condition that is most probably neuropathic with a central component. The condition is also known as stomatodynia, oral dysesthesia, or stomatopyrosis and is often accompanied by dysgeusia and xerostomia. BMD may be subclassified into primary BMD, or essential/idiopathic BMD for which a neuropathologic cause is likely, and secondary BMD, resulting from local or systemic pathologic conditions. By definition, primary BMD cannot be attributed to any systemic or local cause. BMD is, unfortunately, characterized by resistance to a wide range of treatments and is one of the most challenging management problems in the field of orofacial pain. Owing to often vague criteria, the exact prevalence of BMD is unclear. However, it seems that BMD is most common in postmenopausal women, and reported prevalence rates in general populations vary from 0.7% to 15%. The tongue, usually the anterior two-thirds, is the primary location of the burning complaint in the majority of cases. However, usually more than one site is involved; in addition to the tongue, the hard palate, lips, and gingivae are frequently affected. Pain intensity varies from mild to severe; VAS scores reported range from 5 to 7 but may reach 8 to 10.14 The most common terms used to describe the pain quality are ‘‘burning’’ or ‘‘hot.’’ BMD is typically of spontaneous onset and lasts from months to several years. Although a chronic unremitting pattern is usual, spontaneous or partial remission of BMD is reported in 3% to 50% of patients about 5 to 7 years after onset. A possible association to anxiety, depression, and personality disorders is described in the literature, particularly in postmenopausal women, but it is unclear whether pain initiated the psychological disorder or vice versa. Although a minority of BMD patients have significant distress, the vast majority cope better than most chronic pain patients. Secondary BMD may result from local or systemic factors or diseases. Local factors and diseases known to induce secondary BMD include oral candidiasis, galvanism, lichen planus, allergies, hyposalivation, and xerostomia. Systemic disorders known to induce secondary BMD include hormonal changes, nutritional abnormalities (e.g., vitamin B12, folic acid, or iron deficiencies),

V CHRONIC PAIN: NONCANCER PAIN 135

diabetes mellitus, drugs (directly or indirectly), autoimmune diseases, and emotional stress. Successful treatment aimed at the primary disease will usually (but not invariably) alleviate the burning sensation in secondary BMD patients.

Treatment (see Table 17–10) Topical therapies may be useful, particularly in elderly, medically compromised patients. Topical clonazepam (sucking and spitting 1 mg three times daily for 2 wk) was effective in reducing pain intensity in a subgroup of BMD patients, with some residual effect at 6 months. Topical anesthetics may decrease or increase pain such that this is not a predictable mode of therapy. Reduction in pain after treatment with benzodiazepines and lowdose TCAs or other antidepressants appear as case reports. Multiple studies consistently demonstrate the prolonged benefit of a 2-month course of 600 mg daily of a-lipoic acid.15 Therapy-resistant BMD has been associated with underlying psychological distress, and these patients may particularly benefit from CBT.

Traumatic TNs After zygomatic complex fractures, residual, mild hypoesthesia of the infraorbital nerve is common but chronic neuropathic pain developed in only 3.3% of patients. This compares with about 5% to 17% in other body regions. Persistent pain after successful endodontics was found to occur in 3% to 13% of cases, whereas surgical endodontics resulted in chronic neuropathic pain in 5% of cases.14 Factors significantly associated with persistent pain were long duration of preoperative pain, marked symptomatology from the tooth, previous chronic pain problems or a history of painful treatment in the orofacial region, and female gender. The fact that preoperative pain parameters were important suggests that some form of sensitization may have occurred, predisposing to chronic pain.

Atypical Facial Pain Atypical facial pain (AFP; previously known as persistent idiopathic facial pain) is employed when no other diagnosis is feasible and has, therefore, tended to include a heterogeneous group of patients. Some AFP cases responded to triptans, suggesting migraine-like mechanisms, whereas in others, triptans were ineffective. As knowledge and diagnostic skills accumulated, many AFP cases were classified as chronic myofascial pain, traumatic neuropathy, preor atypical TN, facial migraine, or NVOP. It is likely that much of the collected data on AFP represent a neuropathic condition, and many AFP patients demonstrate some degree of sensory dysfunction. The latest International Headache Society criteria for AFP include the presence of daily or near-daily pain that is initially confined but may subsequently spread.14 The pain is not associated with sensory loss and cannot be attributed to any other pathologic process. This is a rather loose definition that has not been fieldtested and may misleadingly allow the classification of a large number of chronic facial pain disorders. Until specific data on AFP accumulate, we describe in brief the features of AFP. Pain is usually poorly localized, radiating, and mostly unilateral, although up to 40% of patients may describe bilateral pain.14 AFP is commonly described as ‘‘burning,’’ ‘‘throbbing,’’ and often ‘‘stabbing.’’ Severity is mild to severe and rated approximately 7 on a VAS. Most patients report long-lasting (years) chronic daily pain, although there have been reports of pain-free periods. Pain onset is often associated with surgical or other invasive procedures. Although there should be no sensory deficits, these have been reported in up to 60% of cases. The lack of a clear pathophysiologic basis precludes the establishment of a treatment protocol. The use of TCAs and anticonvulsants may be beneficial.

Atypical Odontalgia Many atypical odontalgia cases present with neuropathic symptomatology such as continuous, burning pain, and many report trauma as the initiating event. There are some indications that atypical odontalgia may be a subtype of ATP and that both are neuropathic in origin. Other cases may have a throbbing character to the pain with no demonstrable pathology suggesting neurovascular mechanisms. The lack of precise validated criteria is an obstacle in the characterization of atypical odontalgia.

Complex Regional Pain Syndrome Complex regional pain syndrome (CRPS) has been previously termed sympathetically maintained pain, reflex sympathetic dystrophy, or causalgia. These early terms were based on observations of the clinical phenotype that often suggested involvement of the sympathetic nervous system. However, the link between nociceptive neurons and postganglionic sympathetic activity is inconstant, with sympathetic blocks sometimes altering the syndrome at least temporarily and sometimes not. Adrenergic mechanisms in some form do appear to be involved in some of these conditions, but measurements of sympathetic responses have often shown normal results.14 CRPSs are painful disorders that develop as a consequence of injury. Two subtypes have been defined: CRPS I (previously reflex sympathetic dystrophy) and CRPS II (previously causalgia). Both these entities present with spontaneous pain accompanied by allodynia and hyperalgesia that are not limited to dermatomal regions. Additional signs include edema, abnormal blood flow in the skin, and abnormal sudomotor activity. CRPS I may develop as a consequence of remote trauma or after relatively minor local trauma such as sprains or surgery. These result in minor or no identifiable nerve lesions with disproportionate pain. The less frequent form, CRPS II, is characterized by a substantiated injury to a major nerve and is, therefore, a neuropathic pain syndrome by definition. In both of these syndromes, there may be clinical evidence to support the involvement of the sympathetic nervous system, in which case the term sympathetically maintained pain is added. The historical dependence on sympathetic involvement for the diagnosis of CRPS has probably prevented the identification and documentation of head and neck cases. Thus, the cases reported in the literature have relied on cervical sympathectomy, clonidine, guanethidine, and stellate ganglion blockade to confirm CRPS.14 However, some of the diagnostic criteria are rarely, if ever, observed in post-traumatic orofacial pain. For example, trophic changes and atrophy of skin are unreported in the trigeminal region, and motor disturbances are rare. The other criteria listed are distinctly similar to those described in ATF, atypical odontalgia, and clear posttraumatic cases.

Treatment of Neuropathic Pain (see Table 17–10) The available evidence confirms that the mainstays of neuropathic pain treatment remain the AEDs and the TCAs. The usual endpoint in drug trials has generally been a 50% reduction in pain intensity. However, research has shown that about a 30% reduction represents meaningful pain relief for neuropathic pain patients. The role of surgery in the management of traumatic trigeminal neuropathies is unclear. The literature reveals that some cases have been treated with peripheral glycerol injections with some success, but we have found no prospective controlled trials. No prospective trials appear in the literature on central procedures aimed at the trigeminal ganglion or the dorsal root entry zone for the treatment of such cases. Anecdotal evidence suggests that central procedures, such as dorsal root entry zone lesions, may be useful for recalcitrant cases. AEDs for the treatment of painful neuropathies exhibit varied NNTs. Phenytoin (NNT = 2) is superior to both carbamazepine

136 Chapter 17  OROFACIAL PAIN (NNT = 3.3) and gabapentin (NNT = 3.8), but as a group, AEDs are inferior to the TCAs in the management of painful polyneuropathies. For TN, however, anticonvulsants remain the drugs of choice, particularly carbamazepine with an NNT for substantial relief of 2.6. Based on the efficacy of pregabalin and gabapentin in peripheral neuropathies, they may also be good treatment options in traumatic neuropathy. Analgesic trials with TCAs reveal that drugs with mixed serotonin/ noradrenaline (e.g., imipramine and amitriptyline) or selective serotonin-norepinephrine reuptake inhibition are superior to the selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine or paroxetine. In painful polyneuropathies, TCAs such as amitriptyline have an NNT of 2.2. With dose titration of imipramine, an NNT of 1.4 for may be attained for traumatic neuropathies. SSRIs have an NNT of 7 in painful polyneuropathies. In diabetic neuropathy, selective serotonin-norepinephrine reuptake inhibitors (SNRIs) are efficacious, for example, venlafaxine (NNT = 4) or duloxetine (NNT = 4.1); both have fewer side effects than the TCAs and may be attractive alternatives. The sodium channel blocking agent mexilitene may be useful in traumatic neuropathies (NNT 2.2) but has been largely ineffective in other neuropathic pains.14 TCAs or gabapentin/pregabalin would be the first drugs indicated in peripheral neuropathy. The excellent NNTs for TCAs are counterbalanced by the excellent side effect profile of the newer anticonvulsants. In patients initiated on amitriptyline with problematic side effects, imipramine, desipramine, or the SNRI venlafaxine should be tried. If these fail or are contraindicated, the anticonvulsants gabapentin and pregabalin offer the best chances for success. Similarly, in patients started on gabapentin, treatment failure is an indication for a trial of TCAs/SNRIs. Alternatively, if TCAs/ SNRIs or gabapentin is only partly successful, combination therapy with their counterparts (e.g., venlafaxine and gabapentin, gabapentin and morphine) should be considered. Third-line monotherapy, or add-on therapy, may be attained with opioids or tramadol. Based on their efficacy in postherpetic neuralgia and diabetic neuropathy, newer agents such as duloxetine may prove useful.

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SUGGESTED READINGS Al-Ani Z, Gray RJ, Davies SJ, et al. Stabilization splint therapy for the treatment of temporomandibular myofascial pain: a systematic review. J Dent Educ 2005;69:1242–1250. Ashkenazi A, Levin M. Three common neuralgias. How to manage trigeminal, occipital, and postherpetic pain. Postgrad Med 2004; 116:16–18, 21–24, 31–32 passim. Barden J, Edwards JE, McQuay HJ, et al. Relative efficacy of oral analgesics after third molar extraction. Br Dent J 2004;197:407–411. discussion 397. Bender IB. Pulpal pain diagnosis—a review. J Endod 2000;26:175–179. Benoliel R, Robinson S, Eliav E, et al. Hemicrania continua. J Orofac Pain 2002;16:317–325. Benoliel R, Sharav Y. Paroxysmal hemicrania. Case studies and review of the literature. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;85:285–292. Benoliel R, Sharav Y, Tal M, et al. Management of chronic orofacial pain: today and tomorrow. 922–924, 926–928 passim; quiz 932. Compend Contin Educ Dent 2003;24:909–920. Bergenholtz G, Spangberg L. Controversies in endodontics. Crit Rev Oral Biol Med 2004;15:99–114. Bermejo-Fenoll A, Sanchez-Perez A. Necrotising periodontal diseases. Med Oral Pathol Oral Cir Bucal 2004;9(suppl):114–119;108–114. Brook I. Microbiology and management of periodontal infections. Gen Dent 2003;51:424–428. Daudia AT, Jones NS. Facial migraine in a rhinological setting. Clin Otolaryngol Allied Sci 2002;27:521–525. de Siqueira SR, Nobrega JC, Valle LB, et al. Idiopathic trigeminal neuralgia: clinical aspects and dental procedures. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;98:311–315. Dubinsky RM, Kabbani H, El-Chami Z, et al. Practice parameter: treatment of postherpetic neuralgia: an evidence-based report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2004;63:959–965. Eisenberg E, McNicol ED, Carr DB. Efficacy and safety of opioid agonists in the treatment of neuropathic pain of nonmalignant origin: systematic review and meta-analysis of randomized controlled trials. JAMA 2005;293:3043–3052. Finnerup NB, Otto M, McQuay HJ, et al. Algorithm for neuropathic pain treatment: an evidence based proposal. Pain 2005;118:289–305. Fitzek S, Baumgartner U, Fitzek C, et al. Mechanisms and predictors of chronic facial pain in lateral medullary infarction. Ann Neurol 2001;49:493–500. Goadsby PJ. Migraine: diagnosis and management. Intern Med J 2003; 33:436–442. Graven-Nielsen T, Mense S. The peripheral apparatus of muscle pain: evidence from animal and human studies. Clin J Pain 2001;17:2–10. Gray A, Kehlet H, Bonnet F, et al. Predicting postoperative analgesia outcomes: NNT league tables or procedure-specific evidence? Br J Anaesth 2005;94:710–714. Herrera D, Roldan S, Sanz M. The periodontal abscess: a review. J Clin Periodontol 2000;27:377–386. Liu JK, Apfelbaum RI. Treatment of trigeminal neuralgia. Neurosurg Clin North Am 2004;15:319–334.

V CHRONIC PAIN: NONCANCER PAIN 137 Martin MV, Longman LP, Hill JB, et al. Acute dentoalveolar infections: an investigation of the duration of antibiotic therapy. Br Dent J 1997; 183:135–137. Matharu MS, Boes CJ, Goadsby PJ. Management of trigeminal autonomic cephalgias and hemicrania continua. Drugs 2003;63:1637–1677. Pareja JA, Cuadrado ML. SUNCT syndrome: an update. Expert Opin Pharmacother 2005;6:591–599. Penarrocha M, Bandres A, Penarrocha M, et al. Lower-half facial migraine: a report of 11 cases. J Oral Maxillofac Surg 2004;62:1453–1456. Polycarpou N, Ng YL, Canavan D, et al. Prevalence of persistent pain after endodontic treatment and factors affecting its occurrence in cases with complete radiographic healing. Int Endod J 2005;38:169–178. Saarto T, Wiffen PJ. Antidepressants for neuropathic pain. Cochrane Database Syst Rev 2005;(3):CD005454. Savage MG, Henry MA. Preoperative nonsteroidal anti-inflammatory agents: review of the literature. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;98:146–152. Scala A, Checchi L, Montevecchi M, et al. Update on burning mouth syndrome: overview and patient management. Crit Rev Oral Biol Med 2003;14:275–291.

Suvinen TI, Reade PC, Kemppainen P, et al. Review of aetiological concepts of temporomandibular pain disorders: towards a biopsychosocial model for integration of physical disorder factors with psychological and psychosocial illness impact factors. Eur J Pain 2005;9:613–633. Svensson P, Graven-Nielsen T. Craniofacial muscle pain: review of mechanisms and clinical manifestations. J Orofac Pain 2001;15:117–145. Swift JQ, Gulden WS. Antibiotic therapy—managing odontogenic infections. Dent Clin North Am 2002;46:623–633, vii. Tidwell E, Hutson B, Burkhart N, et al. Herpes zoster of the trigeminal nerve third branch: a case report and review of the literature. Int Endod J 1999;32:61–66. Wiffen P, Collins S, McQuay H, et al. Anticonvulsant drugs for acute and chronic pain. The Cochrane Database of Systematic Reviews. (2005). Available at http://www.mrw.interscience.wiley.com/cochrane/clsysrev/ articles/CD001133/pdf_fs.html (accessed October 2005). Zakrzewska JM, Lopez BC. Trigeminal neuralgia. Clin Evid 2004: 1880–1890.

Chapter 18

magnetic resonance imaging (MRI) may not be associated with symptomatology. Cervical cord impingement by protruding disks was seen in MRIs of the larynx in 26% of asymptomatic patients over 64 years of age.

NECK PAIN Susan Elizabeth Opper

PATHOPHYSIOLOGY

INTRODUCTION Neck pain is a very common clinical malady with a lifetime prevalence of 40% to 70%. Less common than low back pain, neck pain may be a challenging dilemma for the practitioner, especially in the traumatic setting. Whiplash injuries may lead to severe disability despite a paucity of radiologic abnormalities and a lack of response to treatment. Spontaneous neck pain is usually the result of cervical spine disease, but various organ structures in close proximity may cause referred neck pain. The therapy of neck pain is as varied as its etiology, with choices among pharmacologic, physical, interventional injection, and surgical techniques. Newer treatments include botulinum toxin injections and radiofrequency ablation, whereas the ancient technique of acupuncture is gaining more acceptance for the treatment of refractory conditions.

EPIDEMIOLOGY Severe neck pain will be experienced by 10% of adults within a given year. Women are at increased risk, as are the elderly and those who have been involved in rear-end automobile accidents. Refractory cases are associated with work dissatisfaction and psychological stressors. Poor self-assessed health, a past history of lumbar pain, and number of children are also correlated with neck pain. Cervical spine abnormalities increase with age. Thirteen percent of men over 20 years of age will have spondylosis, whereas 98% over age 70 years will be affected. Abnormalities of the spine revealed on

Neck pain may be spontaneous or traumatic in origin. Soft tissue and cervical spine disease are the most common causes of neck pain. Soft tissue structures include fascia, ligaments, tendons, and muscles. Disorders of the synovial joints and intervertebral disks of the cervical spine may contribute to neck pain as well as refer pain into the posterior head, the shoulder, and distally into the arm (Table 18–1). Cervical radiculopathy refers to loss of neurologic function such as sensory or motor loss or impaired reflexes due to nerve root compression or inflammation. The cause is often cervical disk herniation but may also be secondary to abnormalities of the vertebral column such as spinal stenosis and facet arthrosis. Diabetes and tumor may also cause secondary radiculopathy. Visceral structures that may refer to the neck include the esophagus, thyroid, lymphatics, stomach, lung, and heart. The history and physical examination may provide important clues for determining the etiology. Connective tissue and autoimmune diseases such as polymyositis, ankylosing spondylitis, and rheumatoid arthritis may affect the muscles and joints of the neck and shoulder with resultant pain. Brachial plexus abnormalities and shoulder impingement may also refer to the neck. Whiplash injury was first described in 1928, referring to the cervical spine’s lashlike effect after a rear-end motor vehicle accident. The acceleration/deceleration incident causes extreme flexion and subsequent extension of the neck. Damage to the ligaments, muscles, and joints of the cervical area may ensue. Neck pain and stiffness may be accompanied by headache, dizziness, and memory and concentration disturbances. A chronic pain syndrome that is extremely resistant to treatment may develop in over 10% of whiplash patients. Some pose that secondary monetary gain impedes recovery. The effect of expectation may also play a role because those who do not expect to become better usually do not.