CHAPTER 67 FACIAL PAIN - Semantic Scholar...225. Takahashi SK, Suzuki M, Izuha A, et al. Two cases...

Part IV: Pain Conditions20

221. Bagatzounis A, Geyer G. [Lateral pharyngeal diverticulum as a cause of supe-rior laryngeal nerve neuralgia] Laryngorhinootologie. 1994;73(4):219–221.

222. O’Neill BP, Aronson AE, Pearson BW, et al. Superior laryngeal neuralgia:carotidynia or just another pain in the neck? Headache 1982;22(1):6–9.

223. Johnson DL. Intractable hiccups: treatment by microvascular decompressionof the vagus nerve. Case Report. J Neurosurg 1993;78(5):813–816.

224. Resnick DK, Jannetta PJ. Hyperactive rhizopathy of the vagus nerve andmicrovascular decompression. Case report. J Neurosurg 1999;90(3):580–582.

225. Takahashi SK, Suzuki M, Izuha A, et al. Two cases of idiopathic superiorlaryngeal neuralgia treated by superior laryngeal nerve block with a highconcentration of lidocaine. J Clin Anesth 2007;19(3):237–238.

226. Kunc Z. Treatment of essential neuralgia of the ninth nerve with selectivetractotomy. J Neurosurg 1965;23:494–500.

227. Trescott AM. Headache management in an interventional pain practice. PainPhysician 2000;3(2):197–200.

228. Sjaastad O, Stolt-Nielsen A, Pareja JA, et al. Supraorbital neuralgia. On theclinical manifestation and a possible therapeutic approach. Headache 1999;39(3):204–212.

229. Lambert WC, Okorodudu AO, Schwartz RA. Cutaneous nasociliary neural-gia. Acta Derm Venereol 1985;65(3):257–258.

230. Spokoinaia VA. Neuralgia of the trigeminal nerve and pterygopalatine gan-glion as a complication of paranasal sinusitis [in Russian]. Vestn Otorinolarin-gol 1989;4:49–53.

CHAPTER 67 ■ FACIAL PAINSTEVEN J. SCRIVANI, NOSHIR R. MEHTA, DAVID A. KEITH, M. ALAN STILES,RAYMOND J. MACIEWICZ, AND RONALD J. KULICH

INTRODUCTIONFacial pain syndromes are common in clinical practice. Many ofthese syndromes are also unique, given the complex anatomy andspecialized sensory innervation of the head, face, and neck, andso can pose diagnostic challenges.

The common descriptive terms for facial pain complaints arefrequently misleading. To avoid confusion, clinicians should befamiliar with the International Headache Society’s DiagnosticClassification for Head, Face, and Neck Pain Disorders (Tables67.1 through 67.6).1 Clinicians need to be able distinguish amongpainful conditions that arise from structural pathology, head-ache syndromes, oral and facial structures, temporomandibularjoint disorders, myofascial pain disorders, and primary cranialneuralgias.

TABLE 6 7.1

INTERNATIONAL HEADACHE SOCIETYINTERNATIONAL CLASSIFICATION OF HEADACHEDISORDERS II

14 CATEGORIES• The Primary Headaches: 1–4• The Secondary Headaches: 5–12• Cranial Neuralgias, central and primary facial pain and other

headache disorders: 13–14

Adapted from Headache Classification Subcommittee of the InternationalHeadache Society. The International Classification of Headache Disorders:2nd edition. Cephalalgia. 2004;24(Suppl 1):9–160.

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231. Ahao Y, Li H, Cai Q, et al. Partial middle turbinatectomy and folded fornasociliary neuralgia by transnasal endoscopic surgery, [in Chinese]. LinChauang Er Bi yan Hou Ke Za Zhi 2004;18(2):91–92.

232. Rath EM. Surgical treatment of maxillary nerve injuries. The infraorbitalnerve. Atlas Oral Maxillofac Surg Clin North Am 2001;9(2):31–41.

233. Mathew NT, Kailasam J, Meadors L. Botulinum toxin type A for the treat-ment of nummular headache: four case studies. Headache 2007;48(3):442–447.

234. Tatli M, Keklikci U, Aluclu U, et al. Anesthesia dolorosa caused by penetratingcranial injury. Eur Neurol 2006;56(3):162–165.

235. Stillman M. Clinical approach to patients with neuropathic pain. Cleve ClinJ Med 2006;73(8):726–739.

236. Wallace MS. Pharmacologic treatment of neuropathic pain. Curr Pain Head-ache Rep 2001;5:138–150.

237. Lazorthes Y, Sol JC, Fowo S, et al. Motor cortex stimulation for neuropathicpain. Acta Neurochir Suppl 2007;97(Pt 2):37–44.

238. Brown JA, Pilitsis JG. Motor cortex stimulation for central and neuropathicfacial pain: a prospective study of 10 patients and observations of enhancedsensory and motor function during stimulation. Neurosurgery 2005;56(2):290–297.

239. Levy RM, Lamb S, Adams JE. Treatment of chronic pain by deep brain stimu-lation: long term follow-up and review of the literature. Neurosurgery 1987;21(6):885–893.

ORGANIZATION OF THETRIGEMINAL NOCICEPTIVE

SYSTEMAlthough nociceptive transmission in the trigeminal and spinalsystems is similar, the two systems have important differences.In the perioral region, the trigeminal divisions contain afferentsthat subserve the dermatomes, which include the lips, teeth, gingi-val, anterior two thirds of the tongue, upper pharynx, uvula,and soft palate. In addition to this cutaneous distribution, thetrigeminal nerve contains afferents that provide sensory innerva-tion to a variety of deep structures in the head, including themuscles of mastication and facial expression, the nasal and oralmucosa, the cornea, tongue, tooth pulp, temporomandibularjoint, dura mater, intracranial vessels, external auditory meatus,and ear (partially, and with cranial nerves VII, IX, and X).

The trigeminal system carries somatosensory informationfrom these cutaneous and deep afferent structures as well as fromspecialized organs that have principally nociceptive innervation.

TABL E 67 .2

THE PRIMARY HEADACHES (1–4)

1. Migraine*without aura*with aura

2. Tension-type headache3. Cluster headache and other trigeminal autonomic cephalalgias4. Other primary headaches

Chapter 67: Facial Pain 21

TABLE 67.3

THE SECONDARY HEADACHES (5–12)

5. Attributed to head and/or neck trauma6. Attributed to cranial or cervical vascular disorder7. Attributed to nonvascular intracranial disorder8. Attributed to a substance or its withdrawal9. Attributed to infection

10. Attributed to disorder of homeostasis11. Headache or facial pain attributed to disorder of cranium,

neck, eyes, ears, nose, sinuses, teeth, mouth, or other facialor cranial structures

12. Attributed to psychiatric disorder

TABLE 67.4

HEADACHE OR FACIAL PAIN ATTRIBUTED TODISORDERS OF CRANIUM, NECK, EYES, EARS, NOSE,SINUSES, TEETH, MOUTH, OR OTHER FACIAL ORCRANIAL STRUCTURES (11.1–8)

11.1—Cranial bones11.2—Neck11.3—Eyes11.4—Ears11.5—Rhinosinusitis (Sinus disorders)11.6—Teeth, jaws, or related structures11.7—TMJ disorders (TMD)11.8—Other

TABLE 67.5

CRANIAL NEURALGIAS, CENTRAL AND PRIMARYFACIAL PAIN, AND OTHER HEADACHES (13.1–19)

13.1—Trigeminal neuralgia13.2—Glossopharyngeal neuralgia13.8—Occipital neuralgia

13.12—Constant pain caused by compression, irritation, or dis-tortion of cranial nerves or upper cervical roots by struc-tural lesions

TABLE 67.6

CRANIAL NEURALGIAS, CENTRAL AND PRIMARYFACIAL PAIN, AND OTHER HEADACHES (13.1–19)

13.15—Head or facial pain attributed to herpes zosterpostherpetic neuralgia

13.18—Central causes of facial painanesthesia dolorosacentral poststroke painfacial pain attributed to multiple sclerosispersistent idiopathic facial painburning mouth syndrome

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Most nociceptive afferents relay through the trigeminal brainstemcomplex, with oral and perioral structures represented more ros-trally than peripheral sites on the face.2 In addition, nociceptiveafferents from the other cranial nerves and the upper cervicalspinal segments (C2–C4) also are relayed through the trigeminalbrainstem complex.

In the subnucleus caudalis, cells relaying nociceptive signals(nociceptive-specific cells and wide–dynamic-range cells) are pri-marily localized to analogous regions of lamina I and V in thespinal cord. Deep afferents also converge on cells that also receivecutaneous nociceptive input, providing a substrate for referredpain in the head, face, and neck through the trigeminal system.Finally, the trigeminal nociceptive relay cells are strongly modu-lated by central pathways (descending opioidergic, noradrener-gic, and serotonergic) that may dynamically modulate nocicep-tion under a variety of environmental situations and behavioralstates.2

Although the trigeminal dermatomes do not generally overlapthose supplied by the adjacent cervical spinal nerves and othercranial nerves, they overlap extensively in the spinal afferent sys-tem. Three adjacent spinal roots must be injured to render anyone region anesthetic. In the trigeminal system, under normalconditions, a section of one trigeminal division renders almostthe entire dermatome anesthetic. Because the peripheral sensorynerves overlap so little with the trigeminal system, nerve lesionsmay result in more pronounced central somatosensory changesthan those evoked by similar lesions in spinal nerves. Thesechanges may partly underlie trigeminal neuropathic pain disor-ders. Additionally, the trigeminal system may be developmentallyand functionally distinct as a result of three hypothetical factors:(1) it innervates highly specialized tissues that are engaged inhighly specialized functions; (2) it experiences two develop-mentally unique events: one programmed pain event and oneprogrammed denervation event (eruption and exfoliation ofteeth); and (3) it can be affected by dental surgery proceduresperformed with local anesthesia, which alters the afferent inputinto the system. These factors may also influence the developmentof chronic facial pain.

DIAGNOSTIC EVALUATIONPain in the mouth or face is one of the most common presentingsymptoms in clinical practice. The majority of symptoms are re-lated to dental disease and, in most cases, the cause can readilybe established, the problem dealt with expeditiously, and the paineliminated. However, in a few patients, pain may be persistentand defy attempts at treatment. Intractable oral and facial painscan be diagnostically challenging, given the many potential causesof pain, the anatomic complexity of the region, and the psychoso-cial importance of the face and mouth. A rigorous protocol forevaluating these patients includes a thorough history and an ap-propriate clinical examination (see Chapter 17).

A detailed history should always be obtained before examin-ing the patient or ordering special tests or imaging studies becausethe history will establish a diagnosis in a majority of cases.

Chief Complaint

The patient’s description of the pain may provide clues to itscause. Primary neuralgias are frequently described as sharp andlancinating, secondary neuralgias have a burning quality, vascu-lar headaches are throbbing, and muscle pain is described as adeep and dull ache. The patient may not be able to give all thesedescriptions at the first interview, and corroborating informationfrom relatives and friends may be needed to build a general pic-ture of the pain as it affects the patient. Each pain complaintshould be listed in order of severity.

AQ1

AQ1AQ1


History of Present Complaint

The intensity of the pain needs to be measured against the pa-tient’s own experience of pain, need for medication, and effecton lifestyle. For example, does the pain interfere with work, sleep,or social activities? How severe is it on a 10-point scale? Does itfluctuate over time? The origin of the pain should be determinedby asking the patient to indicate the site of the pain or the siteof its maximum intensity. Its anatomic distribution should beaccurately traced in terms of local anatomy.

The patient should be encouraged to remember the eventssurrounding the onset of the pain, even if it was several yearsago. Any other instance of similar pain should be ascertained,even though the patient may not associate these with the presentproblem. The time relations of the pain should be clarified interms of duration and frequency of attacks, as well as possibleremissions.

Aggravating factors should be determined. Is the pain aggra-vated by the ingestion of specific foods or beverages, by lyingdown, during times of stress, talking, brushing the teeth, shaving,applying make-up, or by other identifiable factors? In addition,relieving factors (e.g., lying down, sleeping, heat, and cold) areimportant clues.

The effects of previous treatments need to be clarified. Whichmedications have helped? Has surgery altered the nature of thepain? Has endodontic treatment or extraction affected the pain?Finally, the presence or absence of associated factors (e.g., swell-ing of the face, flushing, tearing, nasal congestion, or facial weak-ness) needs to be ascertained.

Medical History

Take a detailed history of the patient and the reported pain. Espe-cially, note any trauma to the head, face, and mouth. Identifycurrent and past medications, relevant family history, and the useof over-the-counter medications, supplements, and alternative orcomplementary therapies. Identify any jaw habits, such as clench-ing, grinding, posturing the jaw, or gum chewing, including occu-pational or vocational habits (e.g., playing a wind instrument,scuba diving, and so on). A comprehensive psychosocial historyis imperative for all patients with chronic pain disorders (seeChapter 21). Establish the details of any pending or planned dis-ability claims or litigation (see Chapter 22).

Physical Examination

The purpose of the physical examination is to discover any possi-ble anatomic or physiologic basis for the pain; therefore, it isimportant to proceed systematically. Patients with facial painshould have a complete head and neck examination, not an exam-ination directed by a presumed diagnosis.

Neurologic FunctionThe most important evaluations are of those of the cranial nerves(CN) V (trigeminal) and VII (facial) and the upper cervical nerves(C2–C4). The three divisions of the trigeminal nerve—supraorbi-tal, infraorbital, and inferior alveolar nerves—supply the major-ity of sensation to the mouth and face. Examine the skin distribu-tion of all three divisions, as well as the intraoral distributionof the second and third divisions. Directional sense, two-pointdiscrimination, and sensory perception with von Frey hairs mayhelp with the diagnosis. Heat, cold, and taste may need to betested in certain situations. Pain to pressure over the six foraminamay indicate trigeminal involvement. Corneal and gag reflexesshould be assessed. The size and strength of the masticatory mus-

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cles reflect the motor division of CN V. Facial nerve function canbe assessed by asking the patient to whistle, purse the lips, smile,close the eyes, and frown.

Upper cervical nerve sensation can be assessed on the scalpfor C2 and at the angle of the jaw and upper neck for C3. Pressureover the midsuperior nuchal line directly affects the greater occip-ital nerve and may reproduce the headache in occipital neuralgia.

Because of the overlap of CNs V, VII, IX, and X and theirconvergence on the spinal trigeminal nucleus, a more detailedexamination of these nerves may be necessary. CN IV and VInerve palsies may indicate increased intracranial pressure.

Muscle Function

Pain in the masticatory muscles, face, posterior cervical spine, andupper back (the suprascapular and pectoral girdle) are commoncauses of head, face, and neck pain, so the neck, shoulder, andmasticatory muscles should be thoroughly assessed. The size ofthe muscles can be assessed visually (e.g., temporal hollowing,masseteric hypertrophy). The muscles should be palpated, triggerpoints noted, and head and neck posture should be assessed.A more thorough evaluation of the masticatory muscles includesmeasuring the maximum interincisal opening and lateral andprotrusive excursions. Tremors and fasciculation should also benoted.

Temporomandibular Joint

Palpate the lateral pole of the mandibular condyle for tendernesswith the mouth open and closed. Course and fine crepitationshould be noted and joint noises auscultated. Clicks and pops andthe position in the opening or closing cycle should be observed.Determining whether or not these are eliminated by separatingthe teeth with a tongue blade or by posturing the jaw forwardwill help focus on the functional importance of these joint noises.

Intraoral Examination

Note how the maxillary and mandibular teeth interdigitate whenthe mouth is closed (dental occlusion) as well as the state of thedentition and oral hygiene. Look for evidence of wear on theteeth, excessive toothbrush abrasion, or palatal erosion from re-petitive vomiting. The health of the oropharyngeal mucosashould be recorded, as well as the moistness of the mucosa andpooling of saliva. The parotid and submandibular glands can bemilked to evaluate the quality and quantity of saliva expressed.The tongue and soft palate should be centered midline and freelymobile. Excessive draping of the soft palate, as seen in sleepapnea, should be noted.

Diagnostic Imaging (see Chapter 19)

Periapical dental films and panoramic maxillofacial radiographsare inexpensive, readily available, do not expose patients to exces-sive radiation, and offer detailed information about the teeth andjaws. Computed tomography (CT) can provide more detailedimages of the bony structures of the jaws, temporomandibularjoints, and base of the skull. Three-dimensional imaging can behelpful in some instances. Magnetic resonance imaging (MRI) isbest for evaluating the soft tissues and can be used for assessingthe deep oro- and nasopharyngeal anatomy and the internal anat-omy of the temporomandibular joints. In addition, the brain canbe evaluated with MRI with and without gadolinium contrast.MRI studies can help determine whether the vasculature is im-pinging on the trigeminal ganglion, which can cause trigeminalneuralgia.

Bone scan with technetium-99m will highlight areas of meta-bolic activity within the bone and can help identify areas of infec-tion, tumor extension and continued growth, or degenerativechange in the temporomandibular joint.

AQ1


Laboratory Studies

Routine blood tests include complete blood count and differentialto exclude anemia and blood dyscrasias. Erythrocyte sedimenta-tion rate may be elevated in temporal arteritis. Rheumatoid factorand Lyme titer may be helpful in evaluating temporomandibularjoint disease.

FACIAL PAIN DISORDERS

Pain Attributed to Disorders of theOral Cavity

Facial Pain of Dental Origin (Odontogenic)Tooth pulp has a specialized and possibly exclusively nociceptiveinnervation.3 In contrast, periodontal tissues are innervated by awide variety of sensory afferents. Pain of dental origin is ex-tremely variable and can simulate nearly any pain syndrome.Dental pain may be spontaneous or induced in various ways, andit can be intermittent or continuous (Table 67.7). Because of theextreme variability of toothache, all pains about the mouth andthe face should be considered to be of dental origin until provenotherwise.

Dental pain is typically provoked by thermal or mechanicalstimulation of the damaged tooth, but it can also be provokedby light touch, tooth-tooth contact (in eating and talking), andpressure. Dental pain is usually described as an aching sensationand sometimes as throbbing. When mild, it may be felt only asa tenderness or soreness. When severe, it may have a burning orelectric- or shock-like quality.

Patients often cannot localize pain arising solely from the den-tal pulp. They often cannot determine whether the offendingtooth is mandibular or maxillary, much less which tooth is in-volved. The pain is felt diffusely in the teeth, jaws, face, andhead.4 Clinical and radiographic findings of dental decay, frac-tured dental restoration, tooth fracture, or abscess drainage (fis-tula) may confirm dental pain as the source of the complaint(Tables 67.8 and 67.9).

Reversible and Irreversible Pulpitis. Dental pain occurs mostcommonly secondary to dental caries, which represent a loss ofintegrity of tooth enamel. When enamel integrity is sufficientlybreached, sensitivity to cold or sweet stimulus may result. Cariousprogression occurs more rapidly with dentinal involvement. Atthis stage, the vital dental pulp is exposed to the oral environment,and inflammatory changes in the pulpal tissue are evident histo-logically.

TABLE 67.7

DENTAL AND ORAL SURGICAL CONDITIONS

Dentoalveolar Pathology*pulpal*periodontal

Odontogenic and Nonodontogenic PathologyTrigeminal Neuralgia and ‘‘Equivalents’’Headache and Neck painTemporomandibular DisordersOral Mucous Membrane DiseaseOral Manifestations of Systemic DiseaseNeuropathic Pain (Persistent Idiopathic Facial Pain)‘‘Burning Mouth/Tongue Syndrome’’

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TABLE 67.8

FEATURES OF ODONTOGENIC PAIN

Presence of etiologic factors for an odontogenic origin of painUnilateral painLocalized pain (diagnosis-specific)Pain qualities (sharp, dull, aching, throbbing)Sensitivity to temperatureSensitivity to pressure, palpation, percussionPain reduction by local anesthetic injection??

The pulpal inflammatory process is initially reversible. Revers-ible pulpitis is characterized by inflammation of the pulp thatmay recover or heal when the insult is removed. Continued stim-uli jeopardizes the pulp’s ability to respond and repair itself.Irreversible pulpitis can be distinguished from reversible pulpitisby the duration of symptoms. Both require a stimulus to initiatethe pain; however, the duration of pain is measured in secondsin reversible pulpitis but in minutes or hours in irreversible pul-pitis. Spontaneous odontogenic pain most frequently markspulpal death or necrosis. Pain elicited with heat is most commonlyassociated with pulpal necrosis.5 The general clinical charac-teristics displayed by toothache of pulpal origin are described inTable 67.8.

Cracked Tooth. Incomplete fractures of a vital tooth may triggerintermittent pain when biting on the offending tooth. Risk factorsinclude older age, extensive dental restoration, and parafunc-tional habits, such as teeth grinding. Unfortunately, the cracksare often difficult to find and do not appear on all radiographs.The pain is often confused with that of pulpitis or trigeminalneuralgia, which may result in unnecessary treatment (see Table67.9). Careful clinical examination, including staining or meticu-lous bite tests on each tooth cusp, may be useful.6,7

Acute dental pain typically responds to local treatments (e.g.,ice packs and reduced mechanical stimulation), or systemic non-steroidal anti-inflammatory drugs (NSAIDs). Opioid analgesics(and combinations) are also indicated, depending on the extentof the pain. In many cases, treatment with antibiotics is appropri-ate and palliative until a definitive dental intervention is per-formed. Definitive dental procedures are generally curative.

Disorders of the Periodontium (Periodontal Disease)Chronic periodontal disease is an immune-mediated inflamma-tory process initiated by pathogenic oral microorganisms,8,9 de-stroying either focal or generalized areas of tooth-supportingstructures and the surrounding bone. Chronic periodontitis isgenerally not a chronically painful disorder. Typically, patientsnotice gingival sensitivity and tenderness or gingival enlargementsecondary to inflammation and bleeding with brushing or prob-ing examination. A tooth with lost bone support may have lostthe gingival attachment surrounding the necks and soft tissue ofthe root, which may result in tooth sensitivity, tenderness, andmobility. In acute periodontal infection, tenderness to the touch,erythema, and bleeding may be evident. An acute periodontalabscess may cause swelling and purulence (see Table 67.9). Wheninflammation or infection (i.e., acute pericoronitis) occurs in thesoft tissue or bone around an erupting or partially erupted tooth(particularly third molars, otherwise known as wisdom teeth),similar signs and symptoms may be seen, with pain as a primarycomplaint.

The pain of periodontal disorders also generally responds toNSAIDs, opioid analgesics, or combination analgesics. An acuteabscess may also have to be locally incised and drained. Areasof generalized periodontitis may be treated with tooth scaling and


TABLE 6 7.9

ODONTIC PAIN

Diagnosis Pulpitis Peridontal Cracked Tooth Dentinal

Diagnostic Spontaneous and/or Localized deep Spontaneous or evoke Brief, sharp pain evokedFeatures evoked deep/diffuse continuous pain in brief sharp pain in a by different kinds of

pain in compromised compromised tooth with history of stimulus to the dentindental pulp. Pain may periodontium (e.g., trauma or restorative (e.g., hot or coldbe sharp, throbbing, or gingiva, periodontal work (e.g., crown, root drinks).dull. ligament) exacerbated canal).

by biting or chewing.

Diagnostic Look for deep caries and Tooth percussion over Presence of tooth fracture Exposed dentin orEvaluation recent or extensive compromised may be detectable by cementum due to

dental work. Pain periodontium provokes radiograph. Percussion recession ofprovoked/exacerbated pain. Look for should elicit pain. periodontium. Possibleby percussion, thermal, inflammation or Dental radiographs are erosion of dentinalor electric stimulation abscess (e.g., helpful (periapical structure. Coldof affected tooth. periodontitis, apical taken from different stimulation reproducesDental radiographs dental radiographs angles). pain.helpful (periapical). helpful (bitewings,

periapical).

Treatment Medication: NSAIDs, Medication: NSAIDs, Medication: NSAIDs, Medication: mouthwashnonopiate analgesics. nonopiate analgesics, nonopiate analgesics. (fluoride), desensitizing

Dentistry: remove carious antibiotics, mouth- Dentistry: depends on toothpaste.lesion, tooth washes. level of the tooth Dentistry: fluoride orrestoration, endodontic Dentistry: drainage and fracture-restoration, potassium salts, toothtreatment, or tooth debridement of treatment, or extraction restoration, endodonticextraction. periodontal pocket, of the tooth. treatment.

scaling and root Patient education, diet,planning, periodontal tooth brushing forcesurgery, endodontic and frequency, propertreatment, or tooth toothpaste.extraction.

curettage of the gingival pocketing and possibly local or systemicantibiotic therapy.

Acute Necrotizing Ulcerative GingivitisAcute necrotizing ulcerative gingivitis (ANUG) is an aggressivelydestructive process. The diagnostic triad includes pain, ulceratedor ‘‘punched out’’ interdental papillae, and gingival bleeding. Sec-ondary signs include fetid breath, pseudomembrane formation,‘‘wooden teeth’’ feeling, foul metallic taste, tooth mobility, lym-phadenopathy, fever, and malaise. The cause of ANUG is poorlyunderstood. It appears to be an opportunistic infection in a hostof lowered resistance. The most important predisposing factor ishuman immunodeficiency virus infection and the second, a his-tory of necrotizing gingivitis. Other contributing factors includepoor oral hygiene, unusual emotional stress, poor diet, inade-quate sleep, recent illness, alcohol use, tobacco use, and variousinfections, such as malaria, measles, and intestinal parasites.Treatment consists primarily of bacterial control. Chlorhexidineoral rinses, professional debridement and scaling, and adjunctiveantibiotic therapy with a soft diet rich in protein, vitamins, andfluids are important in treating and preventing the disease.10

Oral Mucous Membrane DisordersDiseases of the oral mucosa are numerous and have a variety oflocal and systemic causes. Typically, these diseases present withpain and oral mucosal lesions, including vesicles, bullae, erosions,erythema, or red and white patches (Table 67.10). Pain may bea symptom of the primary disease process, secondary to an associ-ated process (i.e., infection), or related to damaged oral mucosa

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(i.e., mouth movements, chewing foods, thermal, chemical) andis often treated with both systemic and local analgesic agents.

Disorders of the Maxilla and MandibleNumerous disorders of the bony substrate of the jaws may presentwith pain. These disorders are generally classified as being ofodontogenic or nonodontogenic origin, cystic, cystic-like, ortumor, and benign or malignant (either primary or metastaticdisease). Often, additional historical or examination findingswarrant further evaluation (i.e., swelling, mass, discoloration,numbness, weakness, bleeding, drainage, tooth loss, or mobility).Pain can be treated symptomatically until a definitive diagnosisis established and definitive therapy is initiated (Table 67.11).

Salivary Gland DisordersDisorders of the three major pairs of salivary glands (parotid,submandibular, and sublingual) and many hundreds of minorsalivary glands in the mouth may also produce pain as a primaryor associated symptom. These disorders are often accompaniedby other signs and symptoms (including swelling, drainage, cervi-cal adenopathy, or generalized signs of systemic infection), de-pending on the cause of the disorder. Disorders of the parotidgland can locally extend to produce otologic symptoms or CN(V, VII, or IX) involvement. Disorders of the submandibulargland may result in symptoms of impaired swallowing or impair-ment of CNs V, IX, XII (Table 67.12).

Burning Mouth-Tongue Syndrome (Oral Burning)Burning mouth-tongue syndrome (BMS) is an idiopathic paincondition of the oral mucous membranes akin to idiopathic neu-


TABLE 67.10

COMMON PAINFUL MUCOSAL CONDITIONS

InfectionsHerpetic stomatitisVaricella zosterCandiasisAcute necrotizing gingivostomatitis

Immune/AutoimmuneAllergic reactions (toothpaste, mouthwashes, topical medications)Erosive lichen planusBenign mucous membrane pemphigoidAphthous stomatitis and aphthous lesionsErythema multiformGraft versus host disease

Traumatic and Iatrogenic InjuriesFactitial, accidental (burns: chemical, solar, thermal)Self-destructive (rituals, obsessive behaviors)Iatrogenic (chemotherapy, radiation)

NeoplasiaSquamous cell carcinomaMucoepidermoid carcinomaAdenocystic carcinomaBrain tumors

NeurologicBurning mouth syndrome and glossodyniaNeuralgiasPostviral neuralgiasPosttraumatic neuropathiesDyskinesias and dystonias

Nutritional and MetabolicVitamin deficiencies (B12, folate)Mineral deficiencies (iron)Diabetic neuropathyMalabsorption syndromes

MiscellaneousXerostomia, secondary to intrinsic or extrinsic conditionsReferred pain from esophageal or oropharyngeal malignancyMucositis secondary to esophageal refluxAngioderma

ropathic pain syndromes. It can be focal (inside of the lips andtongue) or generalized and is typically described as a constant,bilateral, burning, painful sensation. The syndrome generally af-fects middle-aged or older women and has been attributed tonumerous oral disorders (i.e., mucous membrane disease, Sjogren

TABLE 67.11

ODONTOGENIC AND NONODONTOGENICDISORDERS

Odontogenic Cysts and TumorsNonodontogenic Cysts and TumorsMetabolic Bone DiseaseMetastatic Bone DiseaseNeurogenic TumorsVascular Lesions—Hemangiomas and Vascular malformations

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TABLE 67.12

SALIVARY GLAND DISEASE

InflammatoryNoninflammatoryInfectiousObstructiveImmunologic (Sjogren’s Syndrome)TumorsOthers (Red herrings)

syndrome-dry mouth, fungal infections) and systemic diseases(i.e., vitamin deficiencies, diabetes mellitus, immune connectivetissue disorders, vasculitides). More recent evidence suggests thatBMS is more likely a neuropathic pain disorder of either periph-eral or central origin. Some recent taste-testing data and func-tional brain imaging studies support this hypothesis (Table67.13).11–15 Current treatments for BMS focus on this hypothesisand use both topical (oral mucosa) and systemic antineuropathicpain medications (see neuropathic pain section below); however,there is little evidence that such treatments are effective.

Pain Attributed to Disorders of the Eye

Pain in and around the eye is a common presenting problem(Table 67.14). Most ophthalmologic conditions producing eyepain are associated with obvious ocular symptoms, signs, or his-tories that implicate the eye as the origin of pain. Several facialpain and headache syndromes present with ‘‘eye pain’’ as thechief symptom (Table 67.15). In addition, during the history andphysical examination, several signs and symptoms warn of moreserious eye disease and even of potential life-threatening problems(Table 67.16).

History and Ocular ExaminationA complete ocular history should include any prior visual loss,ophthalmic diseases (e.g., corneal infections, uveitis, and glau-coma), use of contact lenses, recent or remote ocular surgery, andocular trauma. In addition to noting the specific features of painwhen taking the history for eye pain, such as time of onset, sever-ity, exacerbating and palliating factors, radiation, quality, dura-tion, and frequency, ask about the specific location of pain; forexample, intraocular, retrobulbar, periocular, or frontal and as-sociated symptoms, such as tearing, loss of vision, double vision,photophobia, and discharge.16

Simple instruments are required to perform the basic eye ex-amination, in which the pain specialist can triage patients witheye pain and identify those who require formal ophthalmologicconsultation. Such equipment includes a near vision card (Snellencard), a hand light, and a direct ophthalmoscope. The Snellencard is used to check the visual acuity (VA). The VA should betested using the patient spectacle correction and each eye shouldbe tested individually. The pupil response to light, the regularityof the pupil, and relative afferent papillary defect should be evalu-ated using a hand light. Also, examine extraocular motility exam-ination and the eyelids. Use a hand light to assess the conjunctivafor chemosis, injections, and foreign bodies and the cornea forkeratitis, corneal foreign bodies, and lacerations. Evaluation ofthe optic nerve using the direct ophthalmoscope should be suffi-cient to exclude gross optic atrophy, fundoscopic abnormalities,and papilledema.

Ocular and Orbital Causes of Eye PainAlthough a large percentage of patients with headache attributetheir pain to their refractive errors and present with many pairs


TABLE 6 7.1 3

TRIGEMINAL NEUROPATHIC PAIN DISORDERS

Acute and Postherpetic Burning MouthDiagnosis Trigeminal Neuralgia Deafferentation Pain Neuralgia Syndrome

Diagnostic Brief severe lancinating Spontaneous or evoked Pain associated with her- Constant burning pain ofFeatures pain evoked by me- pain with prolonged petic lesions, usually in the mucous membranes

chanical stimulation of after-sensation after tac- the V1 dermatoma. of the tongue, mouth.trigger zone (pain free tile stimulation. Trigger Spontaneous pain Hard or soft palate orbetween attacks). Usu- zone due to surgery (burning and tingling), lips. Usually affectsally unilateral, (tooth extraction) or but may present as dull women age �50 years.affects the V2/V3 areas trauma. Positive and and aching. Occasional(rarely V1). Possible negative descriptors lancinating evokedpain remission periods (e.g., burning, nagging, pain.(for months/years). boring).

Diagnostic MRI for evidence of Etiologic factors such as Small cutaneous vesicles Rule-out salivary glandEvaluation tumor or vasocom- trauma or surgery in or scarring, usually af- dysfunction (xeros-

pression of the tri- the painful area. Order fecting V1. Loss of nor- tomia) or tumor,geminal tract or root MRI if the area is in- mal skin color. Corneal Sjogren’s, candidiasis,(cerebropontine angle). tact to rule-out periph- ulceration can occur. geographic or fissuredRule-out multiple scle- eral or central lesions. Sensory changes in af- tongue, and chemical orrosis, especially in fected area (e.g., hyper- mechanical irritations.young adults. esthesia, dysesthesia). Nutrition and meno-

pause.

Treatment Medication: anticonvul- Medication: anticonvul- Medication: acyclovir Medication: anticonvul-sants (e.g., carbamaze- sants (e.g., carbamaze- (acute phase) anticon- sants, benzodiazepines,pine, gabapentin); pine, gabapentin); vulsants, antidepres- antidepressants; non-antidepressants (e.g., antidepressants; nonop- sants; nonopiate analge- opiate analgesics; topi-amitriptyline, nortrip- iate analgesics; topical sics; topical agents cal agents (e.g., lido-tyline, desipramine); agents (e.g., lidocaine (e.g., lidocaine 5% caine, mouth washes).nonopiate analgesics, 5% patches). patches). Cognitive-behavior: bio-botulinum toxin. Com- Surgery: ablative surger- Surgery: ablative surger- feedback, relaxation,bination of baclofen ies (e.g., rhizotomy, ies (e.g., rhizotomy, coping skills.and anticonvulsants can gamma knife). gamma knife).produce good results.

Surgery: microvascular de-compression of trigemi-nal root, ablative sur-geries (e.g., rhizotomy,gamma knife).

of ‘‘incorrect’’ glasses, correcting the refractive errors helps fewpatients. The eye is rarely the source of headache localized to theeye and orbit without clinical signs, such as red eye, or symptoms,such as decreased vision or a history of eye trauma. If the basiceye history and examination are normal, an intraocular cause forthe pain is less likely. However, in some ocular causes of eyepain, the eye is superficially normal. The pain specialist shouldbe able to recognize the features of these uncommon causes ofeye pain.

Ocular Causes for Eye Pain with a White Eye (‘‘Quite Eye’’).Other causes of eye pain include acute angle-closure glaucoma,anterior or posterior uveitis, posterior scleritis, intraocular tu-mors, optic neuritis, and corneal disorders (Tables 67.17 and67.18).

Glaucoma. Glaucoma may cause acute or chronic eye pain.Glaucoma is a broad term for a large array of clinical disordersthat are characterized by damage to the optic nerve with visualfield defects generally associated with elevated intraocular pres-sure. Pain in glaucoma is entirely a function of the rate of rise ofintraocular pressure, so only acute forms are likely to be pain-ful.17 The aqueous humor is produced by the ciliary body in the

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posterior chamber; it flows through the pupillary aperture andexits the anterior chamber through the trabecular meshwork inthe anterior chamber angle. Disorders of elevated intraocularpressure are of two types: open angle, in which the aqueoushumor can flow through the trabecular meshwork, and angle-closure, in which the iris or some other structure is physicallyblocking access to the trabecular meshwork. These types are fur-ther subdivided into primary and secondary forms.18

Primary open-angle glaucoma is the most common type ofglaucoma and is almost always entirely asymptomatic. Therefore,this form of glaucoma is rarely the cause of ocular pain in patientswith a ‘‘quite eye.’’18 Interestingly, the miotic eye drops used totreat primary open-angle glaucoma are more likely to cause eyeand brow ache. In contrast, acute angle-closure glaucoma is asso-ciated with severe, acute eye pain. Fortunately, it is far less com-mon than primary open-angle glaucoma. Even though patientswith angle-closure glaucoma can have a normal appearing eye,they typically present with a red eye, edematous cornea, blurredvision, a pupil that is often partially dilated, irregularly shaped,and poorly reactive to light, and intense eye pain.19,20 The painmay radiate widely and often is associated with nausea and vomit-ing. Teeth have been extracted to treat this disorder, as well aslaparotomies for the accompanying gastrointestinal complaints.


TABLE 67.14

PARANASAL, PERIOCULAR, PERIAURICULAR, AND HEAD AND NECK CANCER PAIN

Diagnosis Paranasal Sinus Pain Periocular Pain Periauricular Pain Head and Neck Cancer

Diagnostic Bilateral or unilateral Pain or tenderness with Diffuse aching or sudden Variety of symptoms.Features throbbing or pressure or without eye move- pain with or without Pain may be due

frontal area pain, exac- ments, deep orbital aural discharge (e.g., to tumor, nerveerbated by leaning for- pain, and referred otitis media). compression, second-ward or palpitation pain. ary infection, second-over the sinus. ary myofascial pain,

deafferentation,radiotherapy, chemo-therapy.

Diagnostic History of chronic aller- Examine eyelids, lacrimal The area is innervated by Complete evaluation byEvaluation gies, frequent upper function, conjunctiva, multiple cranial and multidisciplinary team,

respiratory infections, and sclera. Ophthal- cervical nerves so com- CT, MRI, endoscopy,sinusitis, headaches of moscopy and ophthal- plete functional and biopsy and surveil-various types, sinus mology referral. Rule- structural exam neces- lance. Treatment coor-surgery out primary headache, sary (e.g., inspect tym- dination by oncologist.

Refer to ear, nose, and temporal arteritis, panic membrane, TMJ,throat specialist for orbital pseudotumor. and myofascial). CTendoscopic and/or CT and MRI invaluablestudy (e.g., sinus opaci- for mastoiditis andfication). cholesteatoma.

Treatment Ear, nose, and throat Proper ophthalmologic Proper ear, nose, and Oncologist evaluationspecialist evaluation/ evaluation and treat- throat specialist evalua- and treatment.treatment ment. tion and treatment. Medication: anticonvul-

Medication: sinusitis- Medication: NSAIDs; Medication: NSAIDs; sants, antidepressants,topical decongestants; nonopiate analgesics; nonopiate analgesics; opiate or nonopiate an-systemic antibiotics. systemic antibiotics, systemic antibiotics, algesics, topical agents,

Chronic sinus pain- topical corticosteroids, topical corticosteroids, muscles relaxants.NSAIDs; nonopiate botulinum toxin across botulinum toxin in se- Surgery: ablative sur-analgesics; topical forehead and glabellar lected cases. geries.agents (lidocaine areas in selected cases. Surgeryspray); anticonvul- Surgerysants, antidepressants;botulinum toxin.

Surgery

TABLE 67.15

HEADACHE AND FACIAL PAIN SYNDROMES WITH EYEPAIN

Cluster headache and cluster-tic syndromeParoxysmal hemicraniaSUNCT syndromeTrigeminal neuralgiaSphenopalatine neuralgia (Sluder’s neuralgia)Ice-pick headacheIce cream headacheHypnic headacheEye pain, headache and lung cancerNonorganic pain and headache (psychosomatic and psychiatric

disorders)

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TABLE 67.16

RED FLAGS FOR A PATIENT WITH EYE PAIN

New visual acuity defect, color vision defect, or visual field lossRelative afferent pupillary defectExtraocular muscle abnormality, ocular misalignment, or di-

plopiaProptosisLid retraction or ptosisConjunctival chemosis, injection, or rednessCorneal opacityHyphema or hypopyonIris irregularityNonreactive pupilFundus abnormalityRecent ocular surgery (�3 months)Recent ocular trauma


TABLE 6 7.1 7

PAIN IN OR AROUND THE EYE: ‘‘QUITE EYE’’ ANDNORMAL EXAM

Cluster headache and cluster-tic syndromeParoxysmal hemicraniaSUNCT/SUNA syndromeMigraine and tension-type headacheIce-pick headache/Ice cream headache/Valsalvaa headacheTrigeminal neuralgiaSinus disease (acute)Teeth, jaws (TMD)Carotid diseaseTemporal arteritisEye pain, headache, and lung cancer

Early diagnosis of this disease is important; key features are sum-marized in Table 67.17.21,22 This disease is easily diagnosed, andpatients should be referred immediately to an ophthalmologistbecause it can usually be quickly reversed.

Corneal Disorders. Corneal abrasion is a scraping away or de-nuding of the corneal surface by external forces on the cornealsurface. Eye pain caused by corneal disease is typically describedas ‘‘scratchy’’ or a ‘‘foreign body sensation.’’ Corneal epithelialdefects typically occur after trauma, after ultraviolet light kerati-tis, in contact lens wearers, or from corneal infections. Some pa-tients with corneal disease may present with no conjunctival signsand with an apparently normal eye; however, most patients havesome visible external findings such as red eye, corneal opacity,or abrasion. A corneal abrasion can cause photophobia and ex-cruciating eye pain that often radiates to other parts of the headand face.17,20 Corneal abrasions are best seen by placing a dropof fluorescein in the eye and looking through a slit lamp using acobalt blue light. If the cornea is abraded, antibiotic ointmentshould be applied.16,23 However, most abrasions are self-limitedand heal within 24 to 48 hours.23

Uveitis. The uveal tracts are the pigmented middle ocular tissue,iris, ciliary body, and choroids. Uveitis could have a pure anteriorinvolvement iritis, which occurs in half the cases. These patientsmay present with eye pain, photophobia, and decreased visionwith a relatively quite appearing eye. The other patients withuveitis have posterior involvement chorioretinitis with inflamma-tion of the ciliary body, the choroids, or both. Posterior uveitisis more likely to cause visual loss than anterior uveitis.24,25

TABLE 6 7.1 8

PAIN IN OR AROUND THE EYE: ‘‘QUITE EYE’’ ANDOPHTHALMOLOGIC FINDINGS

Ocular processes—glaucoma, corneal disease, uveitis, scleritis,intraocular tumors, ocular ischemia, hemorrhage

Processes affecting the optic nerve—optic neuritis, ischemic,compressive or infiltrative optic neuropathy

Orbital processes—tumor, infection, inflammatory, vascular,posttraumatic

Cavernous sinus/retro-orbital processes—aneurysm, tumor, throm-bosis, infection, inflammatory, C-C fistula, posttraumatic

Intracranial processes—tumor, pseudotumor cerebri, infection,inflammatory, vascular, intracranial pressure changes

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Scleritis. Inflammation of the deeper layers of the eye wall,known as scleritis, usually presents with severe, intense, and bor-ing pain.23–25 The pain is often localized to the eye but mayradiate into the sinuses, jaw, or frontal region. The sclera mayappear thin or have a bluish hue, and the globe is usually tender.About half the cases are idiopathic, with other causes includ-ing herpes simplex virus, herpes zoster, and collagen vasculardisease.23

Intraocular Tumors. Primary intraocular tumors typically donot cause pain, but orbital extension of tumors may producetrigeminal involvement (neuropathic pain). Intraocular tumorsmay also produce pain by secondary inflammatory reaction (uve-itis) or elevated intraocular pressure induced by the tumor.

Ocular Causes of Eye Pain with a Red (Inflamed) Eye16,23.Conjunctivitis. Conjunctivitis, or ‘‘pink eye,’’ is the most com-mon cause of a red, irritated eye. Because the conjunctiva hasfewer pain fibers than the cornea, conjunctivitis is generally lesspainful than corneal epithelial defects, and visual acuity is usuallyonly slightly reduced. The three most common types of conjuncti-vitis are viral, allergic, and bacterial. The viral type is often associ-ated with an upper respiratory tract infection, cold, or sore throat,with adenovirus infection being the most common viral cause.The condition is characterized by a watery discharge, mild for-eign-body sensation, and photophobia. Bacterial infection tendsto produce more mucopurulent exudates. Allergic conjunctivitisis extremely common and is often mistaken for infectious con-junctivitis. Itching, redness, and epiphora are typical. The palpe-bral conjunctiva may become hypertrophic with giant excres-cences called cobblestone papillae. Irritation from contact lensesor any chronic foreign body can also induce formation of cobble-stone papillae.

Keratoconjunctivitis Sicca. Also known as ‘‘dry eye,’’ keratocon-junctivitis sicca produces a burning, foreign-body sensation, aswell as injection and photophobia. In mild cases, the eye appearssurprisingly normal, but tear production, as measured by wettingof a filter paper (a Schrimer strip), is deficient. A variety of sys-temic drugs, including antihistamines, anticholinergic, and psy-chotropic medications, cause dry eye by reducing lacrimal secre-tion. Disorders that involve the lacrimal gland directly, such assarcoidosis or Sjogren syndrome, also cause dry eye. Patients maydevelop dry eye after radiation therapy if the treatment field in-cludes the orbit.

Blepharitis. Blepharitis refers to inflammation of the eyelids. Themost common form occurs in association with acne rosacea orseborrheic dermatitis. The eyelid margins are usually colonizedheavily by staphylococci. Upon close inspection, they appeargreasy, ulcerated, and crusted with scaling debris that clings tothe lashes. A chalazion is a painless, granulomatous inflammationof the meibomian gland that produces a pea-like nodule withinthe eyelid. Basal cell, squamous cell, or meibomian gland carci-noma should be suspected for any nonhealing, ulcerative lesionof the eyelids.

Dacryocystitis. Dacryocystitis is inflammation of the lacrimaldrainage system and usually occurs after obstruction of the sys-tem. It can produce epiphora and ocular injection. Gentle pres-sure over the lacrimal sac evokes pain and reflux of mucous orpus from the tear puncta.

Herpes Simplex Infection. Primary ocular infection is generallycaused by herpes simplex type 1, rather than type 2. It manifestsas a unilateral follicular blepharoconjunctivitis and is easily con-fused with adenovirus conjunctivitis, unless vesicles appear onthe periocular skin or conjunctiva. A dendritic pattern of cornealepithelial ulceration revealed by fluorescein staining is pathogno-

AQ1

AQ1


monic for herpes infection but is seen in only a minority of pri-mary infections. Recurrent ocular infection arises from reactiva-tion of the latent herpes virus.

Herpes Zoster Infection. Herpes zoster recurrence from reactiva-tion of latent varicella virus causes a dermatomal pattern of pain-ful vesicular dermatitis, which is covered in detail elsewhere inthis text.

Disorders with Eye and Periocular Pain as the Primary Presentati-on. Several facial pain syndromes present with prominent oph-thalmologic signs and symptoms (Table 67.19). The more com-mon ones are discussed below.

Primary Headache Disorders (see Chapter 61). Many of the pri-mary headache disorders can present with frontotemporal areahead pain or sometimes with periorbital and eye pain (migraine,tension-type headache). Some of these disorders have a primarypresenting symptom of pain in and around the eye (cluster head-ache, paroxysmal hemicrania, conjunctival injection and tearing[SUNCT], and short-lasting unilateral neuralgiform headache at-tacks with autonomic symptoms [SUNA]). In addition to thepain, other signs and symptoms consistent with the diagnosisof a headache disorder are often present (i.e., aura, autonomicphenomenon, etc.).

Carotid Artery Disease. Head, face, and neck pain are frequentlyreported by patients with subarachnoid hemorrhage, intracranialaneurysms, arteriovenous malformations, and carotid and verte-bral artery dissections. Patients describe headache, eye pain, facialpain, and neck pain. Associated symptoms may also be present,depending on the vascular source of the pain.

Subarachnoid hemorrhage can also present with meningis-mus, neck pain, nausea, altered consciousness, and seizure. Theheadache and facial pain is highly variable, ranging from mildpain to the ‘‘first and worst headache of my life.’’

Aneurysms can present with head and face pain with cranialnerve palsies, visual disturbances and sudden blindness, and reti-nal abnormalities. Imaging and lumbar puncture are often war-ranted for the diagnosis before definitive treatment.26

The primary symptom of carotid artery dissection is oftenheadache, either alone or with other symptoms. Frequently, ca-rotid artery dissection also presents with eye pain, facial pain,and neck pain. The headache can be focal or diffuse, whereas thefacial pain is generally ipsilateral. Other findings may be pulsatiletinnitus, visual disturbance, central retinal artery occlusion, andHorner syndrome.

Orbital Inflammatory Pseudotumor. Orbital inflammatorypseudotumor is a pain syndrome thought to be caused by idio-

TABLE 67.19

FACIAL PAIN SYNDROMES WITH PREDOMINANTOPHTHALMOLOGIC FINDINGS

Ocular motor nerve palsyCarotid artery diseaseOrbital inflammatory pseudotumorIncreased intracranial pressure and pseudotumor cerebriIntracranial hemorrhage and strokeIntracranial arteriovenous malformationTrigeminal neuropathiesTolosa-Hunt syndromeRaeder’s paratrigeminal syndromeGradenigo’s syndromePostherpetic neuralgia

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pathic orbital inflammation, which presents typically with eyepain and other orbital findings (proptosis, injection, chemosis,or ophthalmoplegia). The pain may be either unilateral or bilat-eral.16,20,23 Imaging (CT or MRI) typically shows evidence ofidiopathic inflammation, enlargement, and contrast enhancementof orbital structures suggesting pathologic involvement. Orbitalbiopsy may be required to exclude other causes.

Idiopathic Intracranial Hypertension (‘‘Pseudotumor Cerebri’’).Idiopathic intracranial hypertension (‘‘pseudotumor cerebri’’)and facial pain occur primarily in young, obese women of child-bearing age. The common presenting findings are daily headache,transient visual obscurations (seconds), pulsatile intracranialnoises, and double vision.16,20 Typically, visual acuity and colorrepresentation are preserved, but many patients have optic nerve-related, visual-field defects (e.g., enlarged blind spots, generalizedconstriction, and inferior nasal field loss). Several predisposingfactors have been identified, including the use of oral contracep-tives, anabolic steroids, tetracycline, and vitamin A.

Tolosa-Hunt syndrome. Tolosa-Hunt syndrome is an idiopathicinflammatory granulomatous process involving the cavernoussinus. Patients present with painful, steroid-responsive ophthal-moplegia and have episodic, unilateral orbital, or retro-orbitalpain. The ophthalmoplegia (CN II, III, IV, VI) occurs simultane-ously or within the first 2 weeks after the onset of pain. Facialsensation and visual acuity may be diminished.16,27 Other patho-logic conditions should be excluded by physical examination orneuroimaging. Tolosa-Hunt syndrome is thought to be caused anonspecific, granulomatous inflammatory infiltrative processwith no obvious specific pathologic trigger in the region of theposterior superior orbital fissure, orbital apex, or cavernoussinus. The syndrome typically responds quickly (within 72 hours)to treatment with steroids.

Raeder’s Paratrigeminal Syndrome (Paratrigeminal Oculo-Sympathetic Syndrome ). This uncommon facial pain syndromepresents with first division trigeminal neuropathic pain, sensoryloss, or both, sympathetic dysfunction (miosis, ptosis, or both),but with normal forehead sweating (compared to Horner syn-drome). The symptom cluster is localized to the middle cranialfossa medial to the trigeminal ganglion and lateral to the anteriorclinoid process. Neuroimaging is necessary and important and,if negative, should be repeated over a period of time to avoidmissing an underlying abnormality. This syndrome is not specificto any known pathologic condition.20

Herpes Zoster Ophthalmicus (Postherpetic Neuralgia). Herpeszoster ophthalmicus is caused by reactivation of latent herpeszoster virus in the gasserian ganglion, which typically involvesthe ophthalmic division of the trigeminal nerve. Ocular symptomscan occur after zoster eruption in any branch of the trigeminalnerve but are particularly common when vesicles form on thenose, reflecting nasociliary nerve involvement (Hutchinson’ssign). Cranial neuropathies can also occur, usually weeks afterthe skin eruptions.

Temporal Arteritis. Temporal arteritis presents with periorbitalor temporal headache, facial pain, and occasional neck pain.There may be ‘‘jaw claudication,’’ scalp tenderness, and visualloss. The headache is mild to severe and of acute or gradual onset;the patient is typically without a history of headache or of changesin headache pattern. Occulomotor disturbances, dizziness, ver-tigo, and hearing impairment and cervical myelopathy may bepresent, and very frequently, the superficial temporal artery isthickened, nodular, and pulseless.

Patients with temporal arteritis are generally male, smokers,and over age 50. The disorder may be associated with polymyal-gia rheumatica, especially in elderly patients. If untreated or inad-


equately treated, it may result in unilateral or bilateral blindness,brainstem strokes, and transient ischemic attacks. A careful his-tory and physical examination gives a high index of suspicion forthis diagnosis. Additionally, blood studies (elevated Erythrocytesedimentation rate, C-reactive protein) and temporal artery bi-opsy may be necessary. However, biopsies can have false nega-tives as a result of skipped lesions; therefore, bilateral biopsiesare often recommended. Treatment consists of immediate high-dose corticosteroids.

Temporomandibular Disorders

Temporomandibular disorder (TMD) typically presents with fa-cial pain, limited and dysfunctional mandibular movements, tem-poromandibular joint noises (clicking, popping, crepitus), and achange in the way the teeth meet on mouth closure. In addition,reports of eye and periorbital pain, ear pain and stuffiness, head-ache, neck pain, dizziness, and limitation of neck movement areoften present. For a more detailed description of evaluation andtreatments for TMD, see the section on TMD in this chapter.

Pain Referred to the Eye from Intracranial DiseasePain from intracranial diseases, especially those involving thedura and cavernous sinus, may be referred to the eye and orbit.The ophthalmic division of the trigeminal nerve serves the eyeand the orbit. Interestingly, a tentorial-dural branch joins theophthalmic division in the cavernous sinus, receiving sensory in-nervations from much of the intracranial dura, the arteries atthe skull base, and the major venous structures. Inflammation,neoplasm, or ischemia involving intracranial structures maycause pain, which is often referred to as the ipsilateral eye. There-fore, eye pain that remains unexplained after a thorough ophthal-mic evaluation may require neuroimaging to rule out an intracra-nial disorder.16,23,28

Pain Attributed to Disorders of the Ear

Otalgia is defined as pain localizing to the ear. Primary otalgiais pain that originates from the ear (see Table 67.14). Referredotalgia does not have a distinct otologic cause and is also calledsecondary, nonotogenic otalgia. Although earache is a frequentsymptom, systematic population-based studies of the epidemiol-ogy of the different forms of pain associated with diseases of theears have not been conducted. However, 97% of cases of otitismedia present with earache,29 and otalgia was found to be re-ferred in as many as 50% of adults in a general medicine popula-tion.29 An analysis of the symptoms of nasopharyngeal carcino-mas revealed that deafness and earache, encountered in 85% ofpatients, were the most common symptoms beside swelling ofthe throat.30

The cranial and cervical nerves supply sensory innervation tothe ear. The auriculotemporal branch of the mandibular divisionof the trigeminal nerve supplies sensation to the anterior aspectof the auricle helix (including the tragus), the anterior aspect ofthe external auditory canal, and the anterior aspect of the lateraltympanic membrane. The great auricular nerve derived from thecervical nerve plexus (C2 and C3) innervates the remaining partsof the lateral surface of the auricle and the medial surface as well.Afferents from facial, glossopharyngeal, and vagus nerves supplythe posterior aspect of the external auditory canal, the posterioraspect of the lateral tympanic membrane, the posteromedial as-pect of the auricle, and a patch of skin on the mastoid process.The middle ear receives sensory afferents primarily from the glos-sopharyngeal nerve as part of the tympanic plexus. The sensoryafferents of the tympanic plexus are largely formed by Jacobson’sbranch of the glossopharyngeal nerve. The vestibulocochlearnerve does not mediate pain afferents from the inner ear because it

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does not carry pain fibers. Therefore, marked inner ear pathologymay develop without otalgia (see Table 67.14).30,31

In the ear’s embryologic development, the otic vesicles cometo rest between branchial nerves 1, 2, 3, and 4. The sensory andmotor nerves of these arches are CNs V, VII, IX, and X, respec-tively.32–34

Four distinct regions of afferent innervations of the head andneck sites refer pain to the ear: (1) the inferior gingiva, floor ofthe mouth, inferior buccal mucosa, and the anterior two thirdsof the tongue, all of which are innervated by the third branch ofCN V; (2) the tonsillar fossae, lateral bases of the tongue, andsome of the inferior nasopharynx innervated by branches of CNIX; (3) the posterolateral oropharynx, hypopharynx, medial baseof the tongue, and occasionally a small portion of the inferiornasopharynx innervated by mixed branches of CNs IX and X;and (4) the supraglottic larynx and lingual and laryngeal surfacesof the epiglottis innervated solely by branches of CN X.32–34

Otalgia may have otologic (primary) or nonotologic (second-ary) causes. A systemic approach to diagnosis is necessary toprevent overlooking a serious condition and to establish the diag-nosis and proper therapy.

Primary Otalgia

Primary otalgia is pain with a cause in the ear. Usually, it canbe diagnosed by examination of the pinna, auditory canal, andtympanic membrane.

Pinna

Primary pinna pain may be caused by injuries or trauma, suchas lacerations, burns, frostbite, or infections. Persistent minorlesions should be biopsied to rule out underlying malignancy.

External Auditory Canal

Otitis externa, sometimes referred to as ‘‘swimmer’s ear,’’ is aninflammation of the external auditory meatus with resultingedema, otorrhea, pruritus, and otalgia. The otalgia of otitis ex-terna is mediated by sensory afferents of the auriculotemporalnerve, the complex of facial glossopharyngeal and vagus nerves,and the cervical nerves. External otitis arises from acute inflam-mation after an ear trauma, inadequate cleansing of the externalauditory canal, or lengthy contact with liquids in bacterially con-taminated water, especially in lakes or swimming pools. Ear waxbuildup also may be responsible for earache and pressure in theear.

The diagnosis is based on physical examination of the externalauditory canal for edema, erythema, debris (desquamated epithe-lium), and otorrhea. Physical findings may be minimal, with onlyslight edema or hyperemia. In such cases, a history of recent waterexposure or preceding ear instrumentation may be useful. Man-agement includes suctioning of any debris or fluids from the exter-nal auditory canal, treatment with antibiotic and steroid oticdrops, and dry ear precautions.29,35

Malignancy must be considered when evaluating a patientwith otalgia and an apparent refractory otitis externa. A primaryneoplasm of the external auditory canal will too often be misdi-agnosed as an otitis externa, potentially resulting in a costly delayin treatment. Patients with malignant otitis externa may havesevere otalgia, a severe form of otitis externa that has involvedthe bone and marrow of the skull base. It is usually found indiabetics or otherwise immunocompromised patients, so this di-agnosis must be carefully considered in these patients with otal-gia. Timely diagnosis and prompt referral of a patient with malig-nant otitis externa is crucial because progression from boneinvolvement to death is rapid.29,35

Middle EarInfection of the middle ear, otitis media, is likely the most com-mon cause of primary otalgia.36 The pain from inflamed mucosa


in these patients is mediated by way of the glossopharyngealnerve, which supplies sensation to the middle ear and medialaspect of the tympanic membrane. An acute infection of the mu-cous membrane of the middle ear usually stems from an infectionof the upper air passages with dysfunction of the eustachian tube.Rhinitis and adenoid inflammation may also be causes of acuteotitis media. The tympanic membrane will be red and swollen.Occasionally, a purulent discharge is present.

Gradenigo syndrome, defined as the triad of otalgia, otorrhea,and abducens nerve palsy, results from bacterial infection of thepetrous apex air cells. Such an infection causes dysfunction ofthe abducens nerve because it passes through a dural tunnel inproximity to the petrous apex. These complications must be con-sidered in a patient with otalgia and a history of recent otitismedia.

Other Primary CausesPrimary neoplasms arising from within the ear or skull base maycause primary otalgia. Such lesions may originate from the skinof the external ear or from glandular tissues of the external ormiddle ear. A careful otologic and CN examination will helpmake the diagnosis. The sternocleidomastoid muscle attaches tothe mastoid process, and overuse or spasm may manifest as adull, aching otalgia.

Secondary (Referred) OtalgiaIn the absence of otologic factors, the pain is termed secondary,nonotologic, or referred otalgia. The classic definition of referredpain is pathology in one part of the body that gives rise to painin another nonpathologic site. Referred ear pain may result frompathologic factors involving the sensory supply of the CN V, IX,and X and the spinal nerves C2 and C3. Irritation of the sensorybranch of the facial nerve (CN VII) is not true reflex or referredpain. It is usually the initial symptom of Bell palsy or RamsayHunt syndrome, and the diagnostic finding of facial paralysisusually occurs within 24 to 48 hours after the onset of pain.33,34

Trigeminal Nerve Referred Pain. Pain referred to the ear fromthe second and third divisions of the trigeminal nerve is usuallylocated anterior to the tragus and along the anterior wall of theexternal auditory canal, which is supplied by the auriculotem-poral nerve. Any disease process involving the anterior two thirdsof the tongue, the floor of the mouth, gingiva, mandible, anteriorhalf of the palate, teeth, infratemporal fossa, paranasal sinuses,and the submandibular or parotid glands may result in trigemi-nal-nerve referred pain. The most common otalgia of fifth nerveorigin are dental disorders.

Glossopharyngeal Nerve (CN IX) Referred Pain. Referred painover the glossopharyngeal nerve may result from infections, ulcer-ations, and tumors of the palatine tonsil, nasopharynx, eusta-chian tube, posterior half of the palate, and the posterior thirdof the tongue. This pain is usually felt deep in the ear, in contrastto the more superficially located pain mediated by the trigeminalnerve. Such ear pain is frequently the only symptom after tonsil-lectomy and adenoidectomy.

Vagus Nerve (CN X) Referred Pain. Ulcerative lesions due tomalignancy or chronic infections in the larynx or hypopharynxmay irritate the superior laryngeal branch of the vagus nerve,causing pain referred to the ear.

Spinal Nerves C2 and C3 Referred Pain. Pain in the mastoid areaand over the posterior portion of the pinna is mediated by thegreat auricular nerve, which is derived from the spinal nerves C2and C3. The most common cause of cervical pain is trauma tothe cervical spine. Cervical arthritis, cervical disks, cervical tu-mors, and muscle traction headache should be considered in the

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differential diagnosis. The differential diagnosis for referred otal-gia is extensive: the more common causes are described below.

Temporomandibular Disorders. In addition to otalgia, otologicmanifestations of temporal mandibular joint (TMJ) disorders caninclude aural fullness, tinnitus, and vertigo.4,6,37 A study of ap-proximately 450 patients with TMJ pain found that otalgia wasthe presenting symptom in 48%.34 In this study, the TMJ syn-drome (and hence otalgia) was successfully managed with con-servative therapies such as heat, massage, patient education, oc-clusal splints, and pain control.

Eagle Syndrome. Eagle syndrome is defined as otalgia, facialpain, sore throat, globus, or dysphagia secondary to elongationof the styloid process or ossification of the stylohyoid ligament.The abnormal styloid process may produce pain through differentmechanisms, one of which is direct compression and irritationof the trigeminal, facial, glossopharyngeal, or vagus nerves. Thestyloid process is typically 20 to 30 mm long. However, 4% ofthe population has a styloid process longer than 30 mm and ofthese, only 4% are symptomatic. The degree to which an elon-gated styloid process causes pain is somewhat poorly defined andcontroversial.6,38

Gastroesophageal Reflux Disease. A large number of symptomshave been linked to extraesophageal reflux of gastric contents,including laryngitis, hoarseness, pharyngitis, bronchospasm, la-ryngospasm, and chronic cough.39 Gastroesophageal reflux dis-ease (GERD) can cause otalgia by irritating the upper aerodiges-tive tract in the sensory distribution of the glossopharyngeal andvagus nerves. Because these nerves also innervate the ear, irrita-tion and damage from acidic gastric secretions may be perceivedas originating within the ear. The reflux of gastric secretions canalso potentially extend superiorly to the eustachian tubes, irritat-ing the ear directly. The diagnosis of reflux-related otalgia shouldbe considered in all patients with otalgia, a normal otoscopicexam, and other symptoms of GERD. Consultation with a gastro-enterologist may be beneficial in managing these patients.39,40

Neoplastic Process (see Table 67.14). Malignancies of the upperaerodigestive tract and tumors in various sites of the head andneck can cause otalgia. Tumors on the anterior aspect of thetongue can also manifest as otalgia if they affect the chorda tym-pani branch of the facial nerve. Nasal and sinus malignancies maypresent with otalgia secondary to eustachian tube dysfunction ordirect neural involvement. In the latter case, the otalgia is me-diated by the afferents from the posterior lateral nasal nerves byway of the sphenopalatine ganglion, which is associated with thesecond division of the trigeminal nerve. Lesions arising from theinfratemporal fossa can cause otalgia by involvement of Arnold’snerve (the auricular branch of vagus nerve) or Jacobson’s nerve(the tympanic branch of the glossopharyngeal nerve). Many ofthese patients face a costly delay in diagnosis if malignancy is notconsidered as a cause.

Treatment of referred otalgia must be directed specifically tothe relevant local causes. Such causes may include pulpitis, peri-apical dental abscess, glossitis, sinusitis, benign or malignantgrowth in the mouth or sinuses, dental malocclusion, RamsayHunt syndrome, tonsils, hypopharynx, or larynx inflammation,or growths in the nasopharynx or eustachian tube.

Pain Attributed to Disorders of the Nose andParanasal Sinuses (see Table 67.14)

These disorders are grouped together because the paranasal si-nuses communicate with the nasal passages through small ostia.Most important among these disorders is sinusitis as it is com-

AQ2


monly linked to headache by physicians and the general publicalike. ‘‘Sinus trouble’’ as a cause of headache is a source of manycontroversies, including how to name them: ‘‘sinus headache,’’‘‘rhinosinusitis headache,’’ and ‘‘sinogenic facial pain’’ are usedto refer to the same disorder.

RhinosinusitisRhinosinusitis is the inflammation of the nasal passages (rhinitis)and one or more of the paranasal sinuses (maxillary, ethmoid,frontal, or sphenoid). The term is more accurate than ‘‘sinusitis’’because rhinitis usually precedes sinusitis, the mucosa of the noseand sinuses are contiguous, both conditions may involve nasalobstruction and discharge.41,42

Sinusitis is overdiagnosed as a cause of headache and facialpain because of the belief that pain over the sinuses must berelated to the sinus. Many of the 60% of patients with unrecog-nized migraine attribute their symptoms to sinusitis.41,43 Rhino-sinusitis is an uncommon cause of facial pain: more than 80%of patients with purulent secretions visible on nasal endoscopyhave no facial pain, most patients with nasal polyposis do nothave pain, and facial pain persists in a large proportion of patientsafter endoscopic sinus surgery.44–47 Paradoxically, sinus diseasealso tends to be underestimated, and a potentially dangerous con-dition, sphenoid sinusitis, is frequently missed.48

Clinical Features. Diagnostic criteria for rhinosinusitis are de-fined in the ear, nose, and throat literature.49 In this diagnosticscheme, rhinosinusitis is subdivided into acute, recurrent acute,subacute, chronic, and acute exacerbations of chronic. Acute si-nusitis lasts from 1 day to 4 weeks, subacute sinusitis from 4 to 12weeks, and chronic sinusitis for more than 12 weeks. Headache isconsidered a minor criterion for the diagnosis of acute rhinosinu-sitis, and headache in the absence of other diagnostic criteria isnot considered to be diagnostic of sinusitis.41,50,51

Key points in the history of pain secondary to rhinosinusitisare exacerbations of pain during an upper respiratory tract infec-tion, an association with rhinological symptoms, pain that wors-ens when flying or skiing, and pain in response to medical treat-ment. Rhinosinusitis usually presents with facial tenderness andpain, nasal congestion, and purulent nasal discharge. Commonsigns and symptoms include anosmia or hyposmia, pain on masti-cation, and halitosis. Most cases of infectious rhinosinusitis thatlast less than 7 days are viral. Acute bacterial sinusitis in adultsmost often presents with 7 or more days of purulent anteriorrhinorrhea, nasal congestion, postnasal drip, facial or dental painor pressure, and cough, frequently at nighttime. Although ap-proximately 50% of adults have fever and 60% of children haveheadache, headache, facial pain, and fever often are of little valuein diagnosing sinusitis. Williams et al.52 found that maxillarytoothache was highly specific in making the diagnosis of rhinosin-usitis: 93% of their patients with toothache had rhinosinusitis.However, only 11% of their patients had maxillary tooth-ache.52,53

The headaches associated with rhinosinusitis are usually con-tinuous. The location of the pain and the position that improvesthe headache varies on the sinus involved (Table 67.20).

Pain in acute maxillary sinusitis is usually in the cheek, gums,and maxillary teeth on the affected side. Acute frontal sinusitiscauses frontal headache with tenderness over the sinus and onthe medial side of the orbital floor, under the supraorbital ridge,where the frontal sinus is thinnest. Frontal sinusitis can result inbrain abscess, meningitis, subdural or epidural abscess, osteo-myelitis, orbital edema, and orbital cellulitis. Acute ethmoid si-nusitis typically produces pain in between the eyes. Coughing,straining, and lying supine can worsen the pain, whereas keepingthe head upright lessens it. Complications of ethmoid sinusitisinclude meningitis, orbital cellulites, and cavernous sinus throm-bosis.54

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TABL E 67 .20

INTERNATIONAL HEADACHE SOCIETY CRITERIA FORACUTE SINUS HEADACHE

• Diagnostic criteria: pain in one or more regions of the head,face, ears, or teeth.

• Clinical, laboratory, or imaging evidence of acute rhinosinusitis(e.g., purulence in the nasal cavity, nasal obstruction, fever, CT,MRI, or fiberoptic nasal endoscopy findings).

• Simultaneous onset of headache and rhinosinusitis.• Headache lasts �7 days after remission or successful treatment

of acute rhinosinusitis.

It is necessary, therefore, to differentiate headaches caused by rhinosinusitisfrom so-called ‘‘sinus headaches,’’ which are chronic headache attacksfulfilling the criteria for migraine without aura with prominent autonomicsymptoms in the nose or migraine without aura triggered by nasal changes.

Acute sphenoid sinusitis, which accounts for only 3% of allcases of acute sinusitis, is frequently misdiagnosed.48 Althoughsphenoid sinusitis rarely causes headache, it can lead to markedmorbidity and mortality and so must be identified early and man-aged aggressively.

As mentioned above, the cavernous sinus is lateral to the sphe-noid sinus. The cavernous sinus contains the internal carotid ar-teries and the third, fourth, fifth, and seventh CNs. The maxillarydivision of the CN V may indent the wall of the sphenoid sinus.The sphenoid walls can be extremely thin, and sometimes thesinus cavity is separated from the adjacent structure by just a thinmucosal barrier. Because of this proximity, infection may spreadto these structures and present as a central nervous system infec-tion or neurologic catastrophe.48,54

Headache is always present in acute sphenoid sinusitis and itmay be frontal, occipital, or temporal and most commonly is acombination of these locations. Periorbital pain is common andvertex pain is rare. Nasal pain and discharge are present in only30% of cases, and fever occurs in more than 50% of patients.Also, pain or paresthesias in the facial distribution of the fifthnerve and photophobia or eye tearing suggest sphenoid sinus-itis.48 The headache and associated symptoms may lead to a mis-diagnosis of migraine, meningitis, trigeminal neuralgia, or braintumor. A severe, intractable, new-onset headache that interfereswith sleep and is not relieved by simple analgesics should raisethe suspicion of sphenoid sinusitis. Neuroimaging is necessary fora definitive diagnose. Complications include bacterial meningitis,cavernous sinus thrombosis, subdural abscess, ophthalmoplegia,and pituitary insufficiency.48,54

Acute sinus headache is defined by the International HeadacheSociety (IHS) diagnostic criteria in the setting of an infectiousprocess requiring verification through imaging and confirmationby response to appropriate antibiotics. The IHS established thefollowing diagnostic criteria for acute sinus headache (rhinosinu-sitis headache) (see Table 67.20)1:

A. Purulent discharge in the nasal passage, either spontaneousor by suction

B. Pathologic findings on radiographic examination, CT, ortransillumination

C. Simultaneous onset of headache and sinusitisD. Headache location (see Table 67.3 for location of pain with

infection of corresponding paranasal sinus)E. The disappearance of the headache after treatment for acute

sinusitis

These criteria may not be valid for diagnosing sphenoid sinus-itis because the purulent discharge is often missing and headachemay precede sinus drainage. The IHS has not validated chronic


sinusitis as a cause of headache or facial pain unless it relapsesinto an acute stage.

Obviously, the term ‘‘acute sinus headache’’ or what is re-ferred to as ‘‘rhinosinusitis headache’’ in this chapter doesnot address the primary headache disorder with secondarynasal symptomatology, commonly referred to as ‘‘sinus head-ache.’’41,55,56

Plain sinus radiographs can diagnose acute maxillary or fron-tal sinusitis but are often inadequate for ethmoid or sphenoidsinusitis. CT is the optimal imaging study to assess the paranasalsinuses. The mucosa of the normal, noninfected sinus approxi-mates the bone so closely that it cannot be visualized on CT.Therefore, any soft tissue seen within a sinus is abnormal. CTmay reveal mucosal thickening, sclerosis, clouding, or air-fluidlevels. Scans of the sinuses without contrast in the coronal plainare highly sensitive for detecting nasal and paranasal sinus dis-ease, including disease in the ethmoid and sphenoid sinuses.57

The prevalence of reversible sinus abnormalities visualized by CTin patients who have the common cold is high. This fact suggeststhat CT may not be specific for bacterial infections. Anteriorethmoid sinus infection is found in every patient who had frontalor maxillary sinusitis.

MRI is more sensitive than CT in detecting fungal infections.In MRI, T2-weighted images are highly sensitive for detectingretained fluid and inflamed tissue of the sinuses, a fact that maylead to exaggerating the importance of otherwise unremarkablesinus disease, such as mild inflammation, small polyps, and reten-tion cysts. Transillumination and ultrasonography of the sinuseshave low sensitivity and specificity for detecting similar findings.Diagnostic endoscopy with the flexible fiberoptic rhinoscope per-mits direct visualization of the nasal passages and sinus drainageareas.58

Differential Diagnosis. Migraine and tension-type headache areoften confused with true sinus headache because of their similarlocations.43,55,56 Some patients, in addition to having all the fea-tures of migraine without aura, have head pain in the face, associ-ated congestion of the nose, and headache triggered by weatherchanges. These patients do not have purulent nasal discharge orother diagnostic criteria of acute rhinosinusitis. The diagnosticcriteria of rhinosinusitis and migraine are similar. Although facialpressure or pain, facial congestion, and nasal blockages are con-sidered major criteria for rhinosinusitis, headache and fatigue areminor criteria, meaning that these symptoms have less diagnosticvalue but are not necessarily less frequent or less intense. In mi-graine, the seminal emphasis for diagnosis is the severity, quality,and location of a headache associated with gastrointestinal orsensory symptoms. Nasal symptoms, including congestion, facialpressure or pain, and rhinorrhea, are commonly reported symp-toms associated with migraines but are often ignored becausethey are not considered essential for the diagnosis of migraine.Therefore, it is important to differentiate headaches caused byrhinosinusitis from headaches fulfilling the criteria of migrainewithout aura with prominent autonomic symptoms in the noseor of migraine without aura triggered by nasal changes, the so-called ‘‘sinus headaches’’ (Table 67.21).43,55,56

Management (see Table 67.21). Acute rhinosinusitis causes ex-cruciating pain; therefore, analgesia is important. In one study,analgesia successfully treated nearly 80% of patients with maxil-lary sinusitis.59

Emergency treatment goals are to facilitate drainage of thecongested nasal sinuses and to eliminate the pathogenic bacteria.Steam and saline prevent crusting of secretions in the nasal cavityand facilitate mucociliary clearance. Locally active decongestantsprovide symptomatic relief by shrinking inflamed and swollennasal mucosa. Oral decongestants should be used if prolongedtreatment (�3 days) is necessary. These agents are �-adrenergicagonists that reduce nasal blood flow without the risk of rebound

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TABLE 67.21

AN OTOLARYNGOLOGY, NEUROLOGY, ALLERGY,AND PRIMARY CARE CONSENSUS ON DIAGNOSIS ANDTREATMENT OF SINUS HEADACHE

Diagnostic Recommendations:Stable pattern of recurrent, self-limiting headache associated with

rhinogenic symptoms are most likely migraineProminent rhinogenic symptoms associated with fever, purulent

discharge with headache as one of several complaints (pain) islikely rhinogenic in origin

MRI or CT as appropriate based on headache history, patterns,changes, and physical signs

Referral to headache specialist for new onset, frequent headache,headache associated with neurological symptoms or signs, orheadache that does not respond to appropriate therapy (mi-graine or rhinogenic)

Therapeutic Recommendations:Migraine with no evidence of infection should be given a trial

of migraine-specific medication and scheduled for follow-upevaluation

Noninfectious rhinogenic symptoms with headache as a minorcomplaint should be provided with a trial of nasal steroids and/or selective antihistamines and/or oral decongestants

Adapted from Levine HL, Setzen M, Cady RK, et al. An otolaryngology,neurology, allergy, and primary care consensus on diagnosis and treatmentof sinus headache. Otolaryngol Head Neck Surg 2006;134(3):516–523.

vasodilation. Mucoevacuant (guaifenesin) and intranasal steroidsmay improve the symptoms, but antihistamines are not helpful.60

Most patients with rhinosinusitis respond to treatment withantibiotics. Amoxicillin is the first choice, unless the patient hasbeen treated within the previous month or lives in an area thathas a high prevalence of �-lactamase–resistant H influenza. Thereis no clear evidence that culturing purulent secretions contributeto managing acute rhinosinusitis, but obtaining a culture anddefining its antibiotic sensitivity may help, particularly if thereare orbital or intracranial complications.

Acute frontal and sphenoid sinusitis require immediate refer-ral to an otolaryngologist for treatment to avoid intracranial com-plications. Consultation should also be considered when thesymptoms are not relieved with at least two consecutive 2-weekcourses of antibiotics.59

Sometimes rhinosinusitis does not respond to medical treat-ment and surgical intervention is necessary to relieve worseningand excruciating pain. The goal of surgery is to improve sinusdrainage by enlarging the orifices, removing obstructive anatomicstructures, or both. Endoscopic sinus surgery alleviates the facialpain in 75% to 83% of cases,44,60 producing greater improve-ment in headache than in facial pain.

Isolate Rhinogenic Disorders Causing Headache

Rhinogenic headache and facial pain can be caused by septalimpaction or contact, rhinitis (allergic or vasomotor) and nasalpolyps, trauma, intranasal tumors, and septal hematoma. In pa-tients without evidence of acute or chronic sinusitis, nasal polyps,or a tumor, Chow61 found that pain was caused by a septal spurin 12 of 18 patients who had rhinologic sources for their primarysymptom of facial pain or headache.

Deviated Nasal Septum. A deviated nasal septum can producesymptoms similar to those of nasal obstruction. Symptoms maybe marked if the deviation is in the region of the nasal valve.However, deflection of the nasal septum is not important as apossible cause of headache.


Inflammatory Rhinitis. Inflammatory rhinitis is accompanied byrhinorrhea, fever, pain affecting the middle part of the face andthe distribution of the first and second trigeminal branches, andsymptoms of an infection of the upper respiratory tract. Inflam-matory rhinitis differs from allergic rhinitis in having more neu-trophils on a nasal swab, whereas allergic rhinitis will show anincrease in eosinophilic leucocytes.

Allergic Rhinitis. As a rule, allergic rhinitis does not cause pri-mary pain, but it may give rise to acute sinusitis in which facialpain is a secondary development.

Vasomotor Rhinitis. The symptoms of vasomotor rhinitis aresimilar to those of allergic rhinitis but with less sneezing, and thepatient does not test positive for allergies.The pathophysiology in-volves an imbalance between the parasympathetic and sympa-thetic autonomic nerve supply of the nasal mucosa. The formerpredominates, the increased vascularity causing nasalobstruction.

Pain Attributed to TemporomandibularDisorders

TMD are defined as a subgroup of craniofacial pain disordersthat involve the TMJ, the masticatory muscle system, and theassociated head, face, and neck musculoskeletal complex (mus-cles, ligaments, and joints).62 Patients with TMD most frequentlypresent with pain, limited or asymmetric mandibular motion, andTMJ sounds. The pain or discomfort is located around the jaw,TMJ, and the muscles of mastication. Commonly associatedsymptoms include ear pain and stuffiness, tinnitus, dizziness, eyepain, neck pain, arm and shoulder pain, and dysfunction andheadache. In some cases, the onset is acute and symptoms aremild and self-limiting. Other patients experience chronic TMDwith persistent pain in association with a combination of physi-cal, behavioral, psychologic, and psychosocial symptoms similarto those of other chronic pain syndromes.

An estimated 75% of the U.S. adult population has experi-enced one or more of the signs and symptoms of TMD.63 Epide-miologic studies indicate a prevalence of 40% to 75% of adultshaving at least one sign of joint dysfunction and approximately33% of persons having at least one symptom of TMD.64,65 Somesigns appear to be relatively common in the general population;TMJ sounds and deviation on opening occur in approximately50% of healthy people.66 Other signs are relatively rare; limitedmouth opening and occlusal changes occur in fewer than 5% ofthe population.67 These disorders are disorders of middle-agedadults (ages 20 to 50), with women seeking care more than men(female:male ratio ranges from 3:1 to 9:1).68 Despite large num-bers of people experiencing signs and symptoms of TMD overtheir lifetime, only 5% to 10% of these individuals are believedto actually need treatment.

Temporomandibular Disorders: A Triadof Dysfunctions

At least three distinct and separate dysfunctions create or affectthe symptoms described by the TMD patient69:

I. Muscle disorders (myofascial pain dysfunction) are relatedto muscle dysfunction, often leading to muscle spasms, pain,and dysfunction. This type of dysfunction can occur in anyskeletal muscle. The triggering area lies in the fascial cover-ings and attachment zones of the muscles, thus the term myo-fascial. This syndrome is sometimes incorrectly referred toas myofacial pain dysfunction.

II. Temporomandibular joint articular disorder (TMJD) is re-lated to specific problems in the TMJs. These problems may

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range from joint sounds to locking, pain, and degenerativechanges of the joints themselves. Invariably, muscle dysfunc-tion is a secondary effect of true TMJD.

III. Cervical spinal dysfunction is related to the spinal column,vertebrae, and the associated ligaments and muscles. The ma-jority of symptoms not directly related to the jaw musclesare triggered or affected by this syndrome.

TMDs are classified in the eleventh major category of the IHS’sClassification and Diagnostic Criteria for Headache Disorders,Cranial Neuralgias, and Facial Pain as headache or facial painassociated with disorders of the cranium, neck, eyes, ears, nose,sinuses, teeth, mouth, or other facial or cranial structures (seeTable 67.3).1 The American Academy of Orofacial Pain adopteda part of this classification and broadened it to include a morefocused classification of TMD (Tables 67.22 and 67.23). In thisclassification, TMDs are broadly divided into two major groups:the masticatory muscle disorders and the articular disorders.70

The masticatory muscle disorders include myofascial pain, myosi-tis, myospasm, local myalgia, myofibrotic contracture, and neo-plasia. The articular disorders include congenital and develop-mental disorders, disc derangement disorders, temporoman-dibular dislocation, inflammatory disorders, osteoarthritis, anky-losis, and fracture. The most common muscle disorders are local-ized myalgia and myofascial pain syndrome. The most commonarticular disorders are disc derangement disorders and osteoar-thritis.

Treatment of TMD has included, among other therapies, oralorthopedic jaw appliances, occlusal adjustment, prosthetic recon-struction, orthodontic correction, biofeedback, biobehavioralstress management, psychotherapy, nutritional guidance, physi-cal therapy, acupuncture, pharmacotherapy, and surgical man-agement. Each of these techniques is supported by some degreeof success and therefore merits notice. However, the key to suc-cessful treatment is an accurate diagnosis, which relies on know-ing the symptoms and their probable causes on an interdiscipli-nary approach (Table 67.24).

TABL E 67 .22

TEMPOROMANDIBULAR JOINT ARTICULARDISORDERS

Congenital or developmentalAplasiaHypoplasiaHyperplasiaNeoplasia

Disc derangement disordersDisc displacement with reductionDisc displacement without reduction

Temporomandibular joint dislocation

Inflammatory disordersCapsulitis/synovitisPolyarthritides

Osteoarthritis (noninflammatory)Primary osteoarthritisSecondary osteoarthritis

Ankylosis

Fracture


TABLE 67.23

MASTICATORY MUSCLE DISORDERS

11.7.2.1—Local myalgia11.7.2.2—Myofascial pain11.7.2.3—Centrally mediated myalgia11.7.2.4—Myospasm11.7.2.5—Myositis11.7.2.6—Myofibrotic contracture11.7.2.7—Neoplasia

Clinical PresentationThe most common symptom of TMD is muscle pain. It is usuallyaccompanied by restricted movement. Patients often also presentwith reduced jaw opening, as well as impaired range of motionin the cervical vertebrae, shoulders, and arms. Other commonlyassociated symptoms of TMD are listed below.

Headache. Symptoms of TMD-related bilateral head and facepain involve multiple postural muscles, the muscles of mastica-tion, or both. The pain is typically of moderate intensity, dulland aching in quality, and described as deep and constant.71–75

Pain is often exacerbated by use of the affected muscles. Morning

TABLE 67.24

TEMPOROMANDIBULAR DISORDERS

Diagnosis TMJ Articular Disorders Muscle Disorders Myofascial Disorders

Diagnostic Features Pain localized in the preauricular Tenderness of the masticatory Diffused dull or aching painarea during jaw function. muscles. Dull, aching pain affecting multiple groups ofUsually presence of painful exacerbated by jaw function or muscles of the head and neckclick or crepitus during mouth palpation region, as well as other partsopening. Limited opening (�35 of the bodymm), deviated or painful jawmovements

Diagnostic Evaluation Internal derangement of the TMJ Tenderness during palpation of Presence of trigger or tenderwith abnormal function of the the masticatory muscles and points in one or more groupsdisc-condyle complex, and/or tendons. Possible limited range of muscles. Pain can radiatedegeneration of the joint of jaw movement and during to distant areas withsurface. Palpation is painful. passive stretching exam. Can stimulation or not of thePossible joint swelling in acute be associated with a trigger points. Rule outphases. MRI, CT, etc., of the parafunctional habit (bruxism- presence of lupusjoint may rule-out tumors and early morning pain). erythematosus.advanced degenerative stages

Treatment Patient education and self-care Patient education and self-care. Same as muscle disorders.Medication: NSAID, nonopiate Medication: topical and systemic

analgesics. NSAIDs., nonopiate analgesics,Physical Therapy: exercise muscle-relaxants,

program. antidepressants, (usuallyOcclusal splints tricyclic antidepressants),Oral maxillofacial surgery: anxiolytics, anticonvulsants,

arthrocentesis, arthroscopic botulinum toxin, trigger pointsurgery, open surgery injections and vapocoolant

spray.Physical therapy: transcutaneous

electrical nerve stimulation,massage, exercise program.

Occlusal splintsCognitive-behavior: biofeedback,

relaxation, coping skills.

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headaches may be related to nocturnal bruxism or sleep disor-ders,76 whereas increasing pain during the day may be related tomasticatory muscle use or head posture.77

Front of Head. Patients reporting pain in the front of the headoften refer to it as ‘‘sinus headache.’’ The pain is usually accompa-nied by pressure along the upper anterior teeth, bridge of thenose, and behind the eyes. Chronic front of the head pain andfacial pain generally indicate a primary headache disorder, notchronic sinus disease. These symptoms can also be caused by areduced posterior occlusal dimension, causing heavy incisal con-tact, resulting in pain of pressure in the anterior vortex of theface. A band-like feeling of the front of the head can also bebrought about by posterior neck muscle contractions or muscletension of the frontalis muscle.

Side of the Head. Temporal headaches are mainly related to mus-cle contraction and fiber spasm of the temporalis muscle. Thetemporalis muscle has three groups of muscle fibers: anterior,middle, and posterior. The anterior fibers bring the lower jaw upand forward, and the middle and posterior fibers swing the jawto full closure and retract the mandible.

Clenching, grinding, or biting on objects while the jaw is dis-placed anteriorly (edge-to-edge) generally creates pain in the ante-rior temporal group (i.e., the patient has pain in the ‘‘temple’’area). Individuals who work at desk jobs with their heads forwardand down tend to clench and grind in this position because gravity


has a greater affect on the mandible. This condition is furtheraggravated by habits such as pencil or pen biting, pipe smoking,or gum chewing.

Clenching or grinding during sleep or clenching with the jawin a posterior position tends to tire the middle and posterior groupof fibers, and the pain is more posteriorly located. Generally, thetemporalis is affected in any dysfunction of the lower jaw.

Back of Head. Deep, dull pain, constant and aggravating in theback of the head, is usually a result of spasms of the trapeziusand sternocleidomastoid muscles. These muscles are long andstrong, and under tension, they pull on their bony attachmentsto the skull—the occiput and mastoid areas. This pulling leadsto soreness in the bone and to deep dull pain radiating up theback of the head and down the neck. The muscle tension maybe independent of, or secondarily related to, displacement of thecervical and upper thoracic vertebrae.

Face Pain. Pain in the sides of the face or pain described by thepatient as ‘‘sinus’’ pain in the zygomatic or orbital area may alsohave a musculoskeletal origin.69 Clenching, acute or chronicstress, and reduction of dental height related to the loss of poste-rior teeth combined with daytime tooth clenching and acute orchronic stress can create muscle trigger points or muscle fatigue.Patients are often aware of this condition after meals and report‘‘a heavy and tired feeling’’ in the jaw muscles. Face pain relatedto sinuses and other pathologies are discussed separately in thischapter.

Eye Pain. Orbital pain symptoms are often described as unilat-eral, constant, and ‘‘boring.’’ Orbital pain is frequently seen inpatients with TMD that includes pain involving the eye and peri-orbital region.69,78–80 Patients with a history of trauma, chronicupper cervical vertebral subluxations, or nerve root impinge-ments related to the occiput and the atlantoaxial region may pres-ent with orbital symptoms. In addition, entrapment of the greateroccipital nerve at the occiput level can also produce this type ofpain, which is often diagnosed as occipital neuralgia. Orbital painoften responds to physical medicine, along with changes in headposture and mandibular position through the use of dental biteappliances.

Ear Symptoms. Pain, stuffiness, and tinnitus may have a muscu-loskeletal cause.81,82 Mandibular posture in relationship to themaxilla affects the masticatory elevator muscles. The medial pter-ygoid muscles help stabilize the left-to-right balance of the mandi-ble on tooth closure. Innervation from the nerve to the medialpterygoid also supplies the middle ear muscles. The tensor tym-pani and tensor palati are actually one muscle with a raphe thatwraps around the hamulus notch of the maxilla. Growth anddevelopment problems related to the proper expansion of themaxilla can affect eustachian tube function and can precipitatemiddle ear infections in children, as well as ear stuffiness withchanges in pressure in the ear in adults. Maxillary and mandibulardysfunctions aid in the development and maintenance of suchsymptoms.

Tinnitus and other types of ear sounds may also have a periph-eral musculoskeletal cause. Specifically, cervical and mandibularpostural factors are found in patients with tinnitus. A combina-tion of physical medicine and dental jaw appliance therapy hasbeen effective in some cases where trauma or aberrations in child-hood growth and development have affected the proper expan-sion of the maxilla.

Sharp, jabbing ear pain upon movement of the mandible isoften seen in patients who have an internal derangement of theTMJ. Usually this derangement presents unilaterally and ipsi-lateral to the joint in question.

Ear pain and symptoms such as stuffiness in the absence ofpositive otologic findings are among the most common reasons to

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evaluate the patient for dental and maxillomandibular imbalance.Treatment often alleviates or reduces the impact of the symptomson the patient.83–88

Temporomandibular Joint Symptoms. Pain and sounds relatedto the TMJs are very common.89,90 Patients commonly reportclicking or grating noises in the ‘‘jaw joints.’’ Generally, clickingis not accompanied by pain. Grating noises are usually unilateraland accompanied by pain radiating to the ear on movement.These noises may be related to trauma or bruxism in the presenceof missing posterior teeth, resulting in injury or anterior disc dis-placement without reduction ‘‘locking’’ of the temporomandibu-lar joint.

Clicking. Much has been written about clicking of the TMJs.Clicks can be classified as immediate-opening clicking, midopen-ing clicking, late-opening clicking, and reciprocal clicking.

The reason for the click, however, remains the same. Whenthe mouth opens, the condyle hits the back of, and ‘‘clicksunder,’’ the articulator disc. This situation can happen at anypoint during movement, depending on the relative position ofthe condyle and disc.

Typically, the articular disc is attached to the head of thecondyle on the medial and lateral poles. The superior head of thelateral pterygoid is inserted into the anterior portion of the discand soft, elastic tissue borders the disc posteriorly.

This arrangement holds the articular disc in position with thecondyle in various jaw movements. If the joint is anatomicallyhealthy, there cannot be a click. Tearing or stretching of the artic-ulator attachments are a prerequisite for clicking.

Clicking can be caused by acute trauma, such as an automobileaccident, whiplash, or a blow to the face. It can also be causedby chronic microtrauma, such as loss of posterior vertical dimen-sion of occlusion or loss of teeth.

Dental interventions can also create this problem by retrudingthe condyle posteriorly during reconstruction or orthodontic re-trusion. Difficult extractions can also affect the joint-disc as-sembly.

Grating Sounds. Grating sounds generally occur in a later stageof TMJ articular dysfunction, along with articular cartilage de-generation. The disc is either torn and shredded or missing com-pletely. The grating is caused by bone-to-bone friction and usuallyindicates osteoarthritic degenerative changes in the joint.

Locking of the Joint. The jaw lock mainly occurs after clickinghas been evident for a while. The articular disc, which is bicon-cave under normal circumstances, loses its shape and becomesspherical or ball-like if anteriorly displaced for a period of time.In this case, the condyle cannot travel normally along the anteriorwall of the glenoid fossa. The patient perceives this restriction asan inability to open the mouth fully. Sometimes the cartilage mayfold on itself with the same clinical effect.

Hypermobility. Increased movement in the jaw comes when theTMJ ligaments are stretched or torn. This loss of integrity allowsexcessive movement, sometimes to the point of anterior opendislocation in a wide opening movement, such as yawning.

Treatment is often a combination of dental therapies, jaw ap-pliance therapy, and physical medicine and can be supplementedwith treatment for bruxism and stress management through bio-feedback relaxation and sleep medicine.

Neck Pain. Neck stiffness and pain are commonly part of theTMD complex.91–93 Trauma, poor posture, and musculoskeletaltension can have chronic effects on the cervical spine, creatingpain, stiffness, and trigger point flare up in the muscles of thehead and neck. The trigeminal and cervical nerves help maintainhead, neck, and jaw posture.94 Mastication and jaw function relyon all the anterior and posterior cervical muscles. In addition,


mandibular and head postures interact to maintain the airwayspace during function and sleep.

Studies of maxillomandibular position and the cervical spinehave shown that reductions of the vertical dimension of the teethand a deep bite can adversely affect cervical muscle function,leading to chronic stiffness, pain, and reduced range of motion.95

It is therefore important to assess the dental factors in patientswith chronic neck pain.

Arm and Back Symptoms. Patients presenting with TMD mayalso commonly present with shoulder pain: pain radiating downthe arm that may or may not be accompanied by tingling andor numbness. Physical examination often reveals thoracic outletsyndrome, costoclavicular syndrome, vertebral subluxations ornerve impingement of the brachial plexus, and even previouslyundiagnosed rotator cuff injuries.96

Temporomandibular Joint Articular Disorders(see Tables 67.22 to 67.24)

The TMJ is a synovial diarthrodial joint that allows the temporalbone to articulate with the condylar head of the mandible. Thejoint allows for sliding as well as hinge movement of the mandibleduring functional mastication. The condyles are not perfectlyround but are wider medio–laterally than anterior–posteriorly.Individual variations follow functional loads and depend on thethickness of connective tissue layers covering the articulating sur-faces.97,98

The condyles travel within their respective mandibular fossae.Each mandibular fossa or glenoid fossa forms the temporal com-ponent of the TMJ. This component is a concave area on theinferior border of the squamous part of the temporal bone andis also referred to as the articular fossa.99

Between the bones that form the TMJ are interposing discsor articular cartilages.100 Each articular disc is formed of densefibrous connective tissue and divides the joint cavity into twoseparate compartments: the upper discotemporal space and thelower discomandibular space. Both compartments are lubricatedby synovial fluid.101 The inferior surface of the disc is concaveto match the articular surface of the condyle, whereas the superiorsurface of the disc is convex to follow the concave surface of thearticular fossa. The articular disc is firmly attached to the medialand lateral poles of the condyle. The lateral ligamentous attach-ments are relatively thin and weak compared to the medial poleattachments and tend to tear more frequently than the medialligamentous attachments. This weakness is the reason for moreanterior medial than lateral disc displacements.

A B

FIGURE 67.1 A,B. Gross anatomy of the TMJ as seen in sagittal sections. bz, bilaminar zone of disc; c,mandibular condyle; d, intra-articular disc; e, eminence; eac, external auditory canal; f, glenoid fossa; llp, lowerhead of the lateral pterygoid muscle.

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Viewed sagittally, the articular disc is divided into three parts:a thicker anterior section called the anterior band, a middle thin-ner intermediary zone, and a broader posterior band that is thethickest of the three (Fig. 67.1). The thinner intermediary zone,along with the two broader anterior and posterior zones, gavethe articular cartilage its classic bowtie appearance on MRI(Fig. 67.2).

In the adult, the central part of the articular disc is avascularand lacks innervations, which allows for changes in the centralthin part of the disc to occur without pain. The articular disc hasa relatively random arrangement of type I collagen fibers, elasticfibers, and glycosaminoglycans comprised of chondroitin sulfate,dermatan sulfate, and hyaluronic acid. The discs allow for rota-tion in the upper joint compartment and translation in the lowerjoint compartment.102 Thus, rotation is approximately the first22.5 mm of mouth opening, and translation from that point tofull mouth opening ranges from 45 to 55 mm between the frontteeth.102

In each joint, the anterior part of the articular cartilage at-taches to the superior head of the lateral pterygoid muscle, andthe inferior head of the lateral pterygoid muscle attaches into thefovea of the condyle. In humans, this attachment of the superiorhead of the lateral pterygoid is variably inserted into 40% to60% of the articular disc.103 The posterior part of the articularcartilage blends into loose retrodiscal tissue consisting of bloodvessels, loose connective tissue, and nerves.

On mouth closure, the retrodiscal tissue is squeezed like asponge and allows the condyle to be fully seated in its fossa. Asthe mouth opens and the condyles move forward in their respec-tive fossa, the blood vessels in the retrodiscal tissues expand tofill the void left by the translating condyles and their interposingarticular cartilages. This act of a sponge being squeezed and thenbeing filled is repeated during jaw function. This region can beinjured if the mouth suddenly opens and closes as a result of ablow or injury to the mandible. This injury can lead to bleedingin the joint space, followed by pain and limitation of movement.

Congenital or Developmental Disorders. Congenital or develop-mental disorders, such as aplasia, hypoplasia, hyperplasia, andneoplasia, can be odontogenic or nonodontogenic and primarilypresent as esthetic and functional problems. Neoplastic lesions,such as osteomas and osteoblastomas of the bone, produce painin more advanced stages,104 as do other primary tumors, such aschondroblastoma and benign giant cell tumors. The most com-mon metastatic tumors are squamous cell carcinoma, nasopha-ryngeal tumors, and parotid gland tumors, such as adenoid cysticcarcinomas.105


A B

FIGURE 67.2 T1-weighted MRIs of a normal temporomandibular joint in (A) closed mouth position and (B)open mouth position.

Disc derangement disorders or articular disc displacements,by far the most common TMJ articular disorders, are character-ized by an abnormal position of the articular disc relative to thehead of the condyle or temporal fossa. Disc displacement is usu-ally marked by a ‘‘clicking or popping’’ sound in the TMJ whenthe mouth is opened and closed. Pain is initially not part of thepresenting symptoms, as long as there is full function. Disc dis-placements suggest torn or stretched collateral discal ligamentsthat bind the disc to the condyle.

Disc displacements are usually anterior or anteromedial, al-though posterior and lateral displacements have been described.Anterior or anteromedial displacement may be related in part tothe fact that the thinnest discal attachments are on the lateralpole of the condyle, as well as the medial direction of pull bythe lateral pterygoid and the inward condylar movement duringmouth opening.106

Disc Displacement With Reduction. A clicking sound on mouthopening and closing is classified as disc displacement with reduc-tion. The term reduction describes the process of the misaligneddisc temporarily coming back (or slipping back) to its properinterposition between the condyle and fossa during full mouthopening (see Fig. 67.2). On closing the mouth, the disc again

A B

FIGURE 67.3 TMJ disk displacement without reduction.

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displaces as the teeth come closer together. This repetitive, ongo-ing displacement on opening and closing produces a reciprocalnoise (clicks) and is hence termed ‘‘reciprocal clicking.’’ Giventhe very common nature of its occurrence, this displacement mayactually represent a stage of physiologic accommodation thatneed not be treated. Where displacement progresses, the incidenceof intermittent ‘‘locking’’ may increase as a result of the momen-tary impedance of the disc as it follows the path of the condyle.This stage generally occurs as a sequel of a chronic clicking condi-tion in patients who tend to clench and grind their teeth at night(nocturnal parafunction) and who have missing posterior teethwith subsequent overclosure of the bite. The teeth act as the door-stop for the TMJs and support the ultimate position of the TMJon full closure. Good dental vertical dimension without shift onclosure is essential in reducing the risk factors for progression.Bite appliance therapy is effective in treating muscular as well asdisc displacement problems.107–109

Disc Displacement Without Reduction. Progression to the nextstage is sometimes referred to as a ‘‘closed lock.’’ In this stage,the disc has been permanently displaced, and its shape has beendeformed so that it prevents the condyle of the mandible fromtranslating to a full open position (Fig. 67.3). Jaw opening is


usually limited to 22 to 25 mm, or about the length of the tipsof two fingers inserted between the upper and lower incisors.Pain may reduce chewing capacity, the mandible deviates to theside of the lock, the joint becomes inflamed, and normal occlusionor ‘‘bite’’ may be disrupted. MRI is the standard for assessingthe soft tissue of the articular cartilage and its displacement,whereas CT is generally done to assess hard tissue for chronicosteoarthritic or bony changes.110,111

Temporomandibular Joint Dislocation. In TMJ dislocation, oropen lock or condylar subluxation, the condyle translates beyondthe anterior eminence of the articular fossa and becomes trappedin this open-mouth position. Chronic hypertranslation can usu-ally be managed by having the patient physically manipulate thejaw back into position. The patient learns to relax the jaw-closingmuscles and to slip the condyle back into position. The mostcommon subluxation occurs during yawning or opening themouth widely when eating.

If the problem is related to trauma or a sudden acute transla-tion, the subluxation is considered to be an acute dislocation.Acute dislocation requires medical intervention in which the mus-cles are relaxed by anesthesia, analgesics, or injected into themuscles and joint, followed by manipulating the joint downwardand backward to let it slip past the anterior eminence of theglenoid fossa. Follow-up with anti-inflammatory medication, ice,and rest or a dental appliance may be necessary until the acutestage passes.112

Inflammatory Disorders. Capsulitis and synovitis are relativelycommon in the TMJ secondary to macro- or microtrauma, irrita-tion, or infections. These insults are accompanied by pain onmovement and inflammation with extreme tenderness of the TMJor on distraction of the joints. MRI may show effusions in theT2-weighted signal, the teeth may not be brought together com-pletely, and pain may occur in the ear.

Joint inflammation may also be a result of systemic polyarthri-tis. Symptoms are similar to those in other joints of the body andare secondary to connective tissue diseases that affect the samepopulation of patients.

Osteoarthritis (Noninflammatory). Primary osteoarthritis is adegenerative condition of the joints characterized by hard-tissueabrasion and degradation of the articular surface of the condylerelated to overload. The condition is frequently seen in patientswith a long history of missing and unreplaced teeth or in patientswith dentures due to remodeling effects. Remodeling is usuallyslow and generally painless in the early stages. Slow progressionmay remain relatively benign over the life span of the patient.

Primary osteoarthritis is usually identified by radiography,such as a dental panoramic image, tomography, or a dental CTscan and grating (crepitus) noises in the joint during movement(Figs. 67.4 and 67.5). Secondary osteoarthritis is usually associ-ated with a single prior event, such as trauma or infection, or byrheumatoid arthritis. An idiopathic degenerative condition pri-marily affecting adolescent girls is termed condylysis. It is seenas a sudden lysis of the condyle, which can creates a shift of thejaw to the affected side and an anterior open bite. The cause ofcondylysis is not clear but the condition is associated with youngwomen with rheumatoid arthritis.113

Ankylosis. Ankylosis is usually related to joint trauma, with sub-sequent bleeding and restricted mandibular movement. Ankylosismaybe fibrous or bony in nature. Fibrous ankylosis usually isseen in the upper joint compartment as a result of adhesionsforming after a joint bleed and prolonged immobility. The jawstill opens slightly, usually enough to accommodate 1 or 2 fingersplaced horizontally between the central incisors. Bony ankylosishas no movement associated with it. Both conditions may requiresurgical release and postsurgical mobilization.114

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FIGURE 67.4 Sagittal view MRI of osteoarthritis of the temporomandib-ular joint.

Fracture. Trauma to the chin, mandible, or any part of the facemay result in bony fractures of the condylar neck, condylar head,bodies of the mandible and maxilla, and temporal fossa. Un-treated, these fractures will generally result in reduced range ofjaw motion, pain, and fibrosis or bony ankylosis. If the fractureis uncomplicated and results in a nondisplaced fracture fragment,immediate treatment may not be necessary, as long as functionis not compromised (Fig. 67.6).115

Muscular DisordersMuscular pain and dysfunction are the most common symptomsof a patient with TMD. The muscles of the masticatory systemare affected in the same way as other striated skeletal muscles ofthe body. Ligaments, nerves, and muscles all function as a com-plex system to stabilize the head on the shoulders, maintain afunctional airway space, and allow three-dimensional movementof the mandible. This system is called the craniocervical-mandib-ular or the stomatognathic system. Breakdown in this complexand finely tuned system ultimately affects the musculoskeletalsystem, most commonly in the form of muscular disorders leadingto pain in the head, face, and neck.

Myalgia due to Trauma. Masticatory muscles can be injured byacute muscle strain or by direct trauma. It is difficult to com-pletely eliminate movement in the masticatory muscles becauseof the need for speech, swallowing, and chewing. If this is furthercompounded by dental parafunctional activities, the healing pro-cess takes longer.

Soft tissue injury results in bleeding, inflammation, and swell-ing, causing the muscle to respond with myalgia, muscle spasm,muscle splinting, or myositis.116 Myofascial trigger points occurin various combinations in the muscle and are considered byTravell117 to be the primary source of muscular pain.

Injury results in a deep, sharp ache on contraction of the


FIGURE 67.5 Coronal view CT scan of osteoarthritis of the temporomandibular joint.

muscle. Depending on the area of injury, the pain may emanatefrom the tendon attachments (tendonitis), the fascial component(myofascitis), or the body of the muscle (myospasm and myositis).The temporalis tendon attachment to the coronoid process is themost frequent site of masticatory tendonitis.

In acute or chronic internal derangement of the TMJ complex,the muscles that support and move the joints can be secondarilyaffected. Protective muscle splinting helps prevent further injuryto the joint. The injured joint is often immobilized by anteriordisc displacement without reduction (closed lock). Splinting ofthe masticatory elevator muscles is maintained until the joint ishealed.

If the internal derangement is not adequately treated, the mus-cles remain chronically shortened and may eventually undergocontracture.118–120 The combination of acute trauma, loss of pos-terior teeth, and moderate to severe parafunction may bringabout an anterior disc displacement with intermittent locking ofthe TMJ. Patients will often report histories of trauma that arefollowed by a variable period of clicking, progressively increasingin frequency and culminating in an abrupt disappearance and aninability to open the mouth. Differential diagnosis of a patientwho has limited mouth opening must include internal derange-ment as well as muscle trismus.

Myalgia secondary to injury of the cervical spine can causeheadaches, facial pain, and masticatory muscle pain. Affectedmasticatory muscles then affect mandibular position. Mandibu-

FIGURE 67.6 Fracture of the left condyle (arrows) shown on panoramicradiograph.

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lar dysfunction results in tightening the muscles of the cervicalspine, thereby perpetuating the cycle. This interaction is the rea-son that a substantial proportion of TMD patients also presentwith a history of cervical injury. This craniofacial and cervicalsyndrome requires multidisciplinary treatment of both the jawand the neck.121

Disc herniations can affect the cervical muscles through pro-tective splinting, which can eventually lead to chronic posturalchanges. Nerve impingement and nerve root injuries can alsoaffect muscle function. Cervical problems are frequently comor-bidities in TMD patients.121,122

A reduction in the space between the posterior spine of theatlas and the base of the occiput as reported by Rocabado123 maycause pain by compression of the suboccipital tissues. The painwill be perceived as a headache starting from the back of thehead.124

Acute or chronic trauma can shift the occiput-atlas relation-ship and may lead to chronic tension in the suboccipital muscleswith resulting fixation and irritation of nerves C1 and C2. Thepain will be referred from the back of the head to the eye, alongthe side of the head, along the skin over the TMJ, and downalong the angle of the mandible, radiating into the neck.

Rotation of the atlas is commonly seen in patients with TMDsand may be linked to changes in occlusal contact patterns andinstability of mandibular position.125 Osteoarthritic degenera-tion and ligament and muscle injury also occur at this level inacceleration-deceleration injuries.

Hypermobility caused by a disruption of the C1-C2 articula-tion also may result in excessive stretching or kinking of the verte-bral artery and may lead to temporary vertebrobasilar syndromewith symptoms of vertigo, nausea, tinnitus, and visual distur-bances.125

The patient with a combined craniofacial-cervical syndromewill have a history of direct or indirect injury to the head andneck. The injury is usually not a direct trauma to the part, butrather a low-grade impact to the body that suddenly twists, flexes,or extends the neck.

Symptoms may range from headache, nausea, visual distur-bances, neck weakness, and pain, to stiffness accompanied bynoises on rotation, flexion, and extension of the head. Dependingon the level of the initial injury, branches of the cervical andbrachial plexus and the areas they supply can also be affected.


Secondary muscles affected can cause superimposed acute orchronic pain, requiring a specific cervical evaluation.

Depending on how the cervical problem affects the mastica-tory system or vice versa, occlusal appliances may reduce muscletension.125

Myalgia Secondary to Parafunction. Oral parafunction includesbruxism, clenching, lip biting, thumb sucking, and any other oralhabit not associated with chewing, swallowing, or speaking.Bruxism and clenching are the most common activities, with aprevalence of up to 90% in the general population.126–130

In most patients, parafunction is mild and intermittent anddoes not require treatment. Moderate or severe bruxism andclenching can damage oral structures, causing wear of the teeth,breakdown of the periodontium in the presence of inflammation,and internal derangement and muscular dysfunction.130

Bruxism and clenching can create excessive force for extendedperiods, whereas normal tooth contact during chewing and swal-lowing over a 24-hour period is about 20 minutes.131 Parafunc-tional forces exceed normal masticatory forces, and the resultantforce vector is primarily horizontal. Under such conditions, theteeth and periodontium are likely to be damaged. Ironically, mosttreatments are designed to protect the occlusion in function ratherthan in parafunction.

If the teeth, periodontium, TMJ, and muscles are consideredto be ‘‘links in a chain’’ working together for proper function,the parafunction usually disrupts the weakest of these structures.The other structures remain relatively healthy or become second-arily affected. For example, parafunctional wear of the caninesmay shift force to the other teeth. If these teeth are strong enoughto withstand the excessive force, the pathology may shift to theTMJ. The patient can therefore present with both tooth and jointpathology.132–134

Patients may present with pain in the cervical muscles as aresult of chronic bruxism and clenching. Cervical muscle activityis related to occlusal contact. The patient may report restlesssleep, waking up with limited mandibular range of motion, head-ache, facial pain, and neck pain. The pain and stiffness usuallyimprove as the day progresses.

If a patient reports that stiffness and pain increase as the dayprogresses, diurnal activity should be suspected. The patient mayreport marked stress and depression. Palpable muscle sorenesswill primarily affect the elevators and the lateral pterygoid.Clenching on the wear facets by moving the mandible laterally—aprovocation test—will increase the pain.

A testing device known as a Bruxcore can quantify nocturnalactivity (Fig. 67.7).135 A portable electromyographic biofeedbackinstrument has also been used to monitor bruxism.136

FIGURE 67.7 Bruxcore tooth grinding indicator.

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Repeated monitoring on different nights at a sleep laboratoryis the most accurate assessment of parafunction; however, it israrely necessary. Electromyographic analysis may show a higherresting tension level than normal, but tension depends on thespecific type of muscle disorder and the specific muscle beinganalyzed.

Treating the parafunctional activity includes reducing thestress leading to parafunctional activity through biofeedback,stress management, medication, and counseling. The goal is todecrease the parafunction to within the adaptive capacity of theindividual.

Oral structures are best protected with occlusal appliancesworn at night, during the day, or both, to reduce loading onthe TMJ, stress on the dentition and periodontium, and muscleactivity (Fig. 67.8).137

Myalgia Secondary to Postural Hypertonicity. As stated above,the stability and function of the cervical region affects the positionof the mandible relative to the maxilla and depends on the posi-tion of the head on the shoulders. This position is affected bygravity and the functional adaptation of the individual.69

A healthy craniocervical complex stabilizes head positionthrough a series of learned and complex antagonistic muscle in-teractions. Forward head posture (FHP) leads to shortening andgreater tension of the posterior cervical muscles.138 The trapezius,sternocleidomastoid, and deeper muscles contract to prevent thehead from tipping forward, leading to hyperactivity and chronictension.

Chronic hyperactivity, such as working on a computer or inan office, can cause the shortened muscles to develop triggerpoints and the accompanying symptoms. The cervical spine isforced to adapt to the forces applied by strong cervical muscles,which may affect normal cervical lordosis.138

The body adapts to FHP by rounding the shoulders, leadingto chronic shortening of the pectoral muscles, which furthermaintains FHP. Pectoral muscle tension along with FHP leadsto upper thoracic breathing and tighter intercostal muscles. Theanterior and middle scalenes may entrap the brachial plexus atthe thoracic outlet, or the first rib can be pulled up to the clavicle,resulting in costoclavicular entrapment.138

Mehta and Forgione139 have discussed the effect of chronicFHP and the relative position of the occiput, atlas, and axis withrespect to each other and the craniomandibular complex. FHPand cervical muscle tension can lead to changes in occlusal con-tacts. Analyzing occlusal contact in maximum intercuspationwith the patient in a supine position does not allow an accurateevaluation of occlusion in function. Likewise, measures to im-prove posture and cervical stability should be considered beforedefinitive occlusal therapy is instituted.

Proper positioning during sleep is important for resting thepostural muscles. A patient who habitually sleeps prone with theneck twisted at 90 degrees experiences the same effects as some-one whose head is turned to one side all day long. In people whosleep on their sides with the lower arm outstretched under thepillow and head, the brachial plexus tends to become entrappedat the costoclavicular level. This side position can be stressfulto the cervical muscles and can result in acute torticollis of thesternocleidomastoid muscle. Neck stiffness and trigger points areobserved in patients with sleep habits that involve strained headpositions.

Standing posture may be affected by leg-length discrepancies,hip rotation, and flat feet. Individuals who lean over machineryare likely have cervical and low-back symptoms. Shoes that areunevenly worn or that have extremely high heels affect balanceand tend to cause a secondary protective adjustment of the pos-tural muscles. This adjustment may result in chronic muscularshortening, trigger points, and spasm. Shifts in body posture andcompensatory cervical changes affect mandibular position andtooth contact patterns.69


A B

FIGURE 67.8 A,B. Oral orthosis appliance for the jaws.

Radiographs CT scans or MRI scans may be needed to evalu-ate spinal curvature and to rule out other pathologies.

Short-term exercise can increase range of motion and improveposture, muscle re-education can strengthen the muscles in thetherapeutic postural position, and home exercise programs canmaintain therapeutic postural position.115

Myofascial Pain and Trigger Points. In 1952, Travell and Rin-zler116 introduced the concept of myofascial pain and triggerpoints. They defined a myofascial trigger point as a hyperirritablelocus within a taut band of skeletal muscle located in a muscleor in its associated fascia or tendon. The spot is painful oncompression and can evoke characteristic referred pain and auto-nomic phenomena.116

Trigger points may be active or latent. Active trigger pointsmay cause pain spontaneously or during movement. Latent trig-ger points afflict nearly half of the population by early adult-hood.140 Latent trigger points are usually not painful, but createweakness and restrict movement. Trigger points can be activatedby a sudden overloading contraction, viral infection, cold temper-atures, fatigue, and increased emotional stress.

The complex nature of myofascial trigger points and theircommon presence in acute and chronic muscle dysfunction re-quire an understanding of their clinical features. According toTravell and Simons,140 there are seven such features:

■ local tenderness over the trigger point■ referred pain, tenderness, and autonomic phenomena■ a palpable taut band associated with the trigger points■ a local twitch response of a trigger point in a palpable taut

band■ perpetuation of trigger points■ a therapeutic effect when stretching the muscle containing the

trigger points■ weakness and fatigability of muscles afflicted with trigger

points relative to unafflicted muscles

Myofascial pain often refers to pain at the head and neckand is considered by some to constitute tension-type headaches.Myofascial pain and trigger points of the masticatory musclescan send pain to the eyes, ears, TMJ, and teeth, depending onthe specific muscles. The pain is usually a dull or intense achethat varies daily and is strongly related to posture and muscleactivity. The pain can usually be localized by the patient and canbe indicated on a diagram of the body. Trigger points commonlyaffect the muscles of posture and mastication, and pain may occurin the same dermatome, myotome, or sclerotome. Satellite triggerpoints may occur within the pain reference zone. Clinically,movement is restricted, passive stretching is painful, and strongcontractions markedly increase the pain. Resistive testing revealsweakness from protective splinting.

Trigger points are palpated by rubbing the fingertip lightly

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along the long axis of the muscle. If present, a taut band will belocated first, and then the more sensitive trigger point. Applyingpressure on a trigger point elicits a grimace or an involuntarysound from the patient called the ‘‘jump sign.’’ A snapping palpa-tion of the taut band will produce a latent trigger response con-firming the presence of the trigger point. Final confirmationcomes on reproducing the patient’s pain by digital pressure onthe point.139

Pressure algometers quantify the amount of pressure appliedto the trigger point, which allows the clinician to document theseverity of the trigger point. It may also be used to objectivelyrecord the efficacy of treatment.

Treating myofascial trigger points includes spray-and-stretchtechniques with ethyl chloride or fluoromethane for its coolingeffects, followed by stretching, hot compresses, and range-of-motion exercises. Trigger point injections of procaine (0.5% solu-tion in saline) or lidocaine (2% without epinephrine) have alsobeen the standard in pain management programs (Fig. 67.9).More recently, botulinum toxin (Botox) has been added to thisarsenal.140–144

Other techniques involve ischemic compression for 30 to 60seconds, acupressure, and pharmacologic therapy, including an-algesics, muscle relaxants, antidepressants, and NSAIDs. Physicaltherapy modalities such as myofascial release and craniosacraltechniques, including postural correction and exercise, have also

FIGURE 67.9 Trigger point injection of the masseter muscle.


been effective in managing myofascial trigger points. Stress andnutritional and hormonal factors should also be addressed.137

In case of the masticatory muscles, occlusal appliances maybe used.138 Dental appliances are effective in reducing musclesymptoms and trigger points in mandibular elevators. These ap-pliances are usually flat plane and fully cover either the upper orlower teeth, depending on when they are to be worn.

Muscle Splinting. Muscle splinting is a reflex by which skeletalmuscles stabilize an injured area to protect it from further injury.The involved muscles become hypertonic and painful. The associ-ated feeling of weakness, although alarming to the patient, isa normal protective reaction to discourage moving the affectedpart.

Muscle splinting is often a sequela to muscle injury and followsmyositis. If splinting is protracted, muscle spasm may follow withor without trigger points, leading to a chronic cycle of myofascialpain and dysfunction.140

Initially, injections are not indicated; ice, rest, and relaxationare the basis of acute therapy. Stretching, ultrasound, or lightmassage can be used in the initial stages. Once the muscles havestarted to heal, splinting decreases, at which point therapy toregain mobility can begin. Mobilization techniques, gentlestretching, and range-of-motion exercises are required to preventongoing myospasm, contracture, and atrophy.

Muscle Spasm (Sustained). A muscle spasm is the painful con-traction of a striated muscle caused by trauma, tension, or dis-ease.113,125 The spasm manifests as pain and interference in func-tion. Muscular fiber contractions occur in response to increasedexcitability of alpha motoneurons.

Prolonged muscle spasm is thought to be caused by the is-chemia induced in a skeletal muscle by its continued contraction.The muscle fatigues and lactic acid builds up, leading to the re-lease of bradykinin, causing pain.

In the masticatory musculature, spasm of the masseter or tem-poralis muscle limits range of motion, which in turn causes thejaw to deflect to the ipsilateral side on mouth opening. If a spasmis isometric, the muscle will be rigid and resistant to stretch. Con-dylar position can be affected in true spasm of the elevator mus-cles and may predispose a patient to internal derangement. Aswith all chronic pain, the severe pain and inability to functioncan bring about psychosocial problems.113

Spastic muscles must be differentiated by palpation from: thepainful soft muscle of myositis; relatively normal, albeit painful,muscle splinting; and localized taut bands and areas of myofascialtrigger points. In contrast, a muscle in spasm has a stiff hardsurface that is painfully resistant to stretch.

Electromyographic recordings show high standing tension inthe affected muscle but lower electromyographic activity relativeto the unaffected side. Pressure threshold meters and tissue com-pliance measurements may help identify the muscles in spasm.Thermography is also being investigated for routine diagnosticuse.145–146

Initial treatment should be directed to eliminating the cyclingspasm. The patient should restrict movement to within painlesslimits, but some function is necessary to regain a normal stretchreflex, which helps relax the muscle. In spasm of a masticatorymuscle, the teeth can be disengaged with a stabilization (flatplane) appliance if the mouth can open enough to insert a tempo-rary emergency splint. Splints are thought to work by shuttingoff proprioceptive input from the teeth that may help maintainspastic activity.

Muscle relaxants administered judiciously can help reducedysfunction and spasm and can be adjuncts to other therapy,such as injection of spastic muscles. Spray-and-stretch techniquesand massage and acupressure techniques may also be effective.

As the muscle starts to respond to treatment, stretching and

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range-of-motion exercises will help prevent contractures andbring the muscle back to full function. Ongoing passive jaw mo-tion exercises will help maintain range of motion. In the mastica-tory system, structural factors, such as the bite, should be cor-rected only after the muscle is pain-free and fully functional.138

Myositis. A direct blow to a muscle can trigger a localized in-flammatory response accompanied by swelling, pain, and immo-bilization.138 The main presenting symptoms will be localizedsoreness, swelling, and pain, along with weakness and immobili-zation of the affected structure. Pain is generally dull, deep, bor-ing, and constant. Episodes of sharp pain related to movementof the affected structure may also be reported.

Injury to the head and neck muscles will result in an accompa-nying reduction in neck movement and changes in shoulder heightand head posture as a means of protecting against further trauma.The pain may be perceived by the patient as a headache. Anaccompanying feeling of weakness in the neck may be experi-enced.

Patients with myositis of the masticatory muscles may reportpain in the face or jaw accompanied by a change in the bite withthe inability to chew, swallow, and speak comfortably. Locally,the area may appear swollen and discolored because of extravasa-tions of inflammatory products. An inflamed muscle will presentas a soft, painful mass on palpation. Pain will be associated withactive as well as passive movement of the affected structure. Theskin may be warmer to the touch than the surrounding area. Thepatient may present with low-grade fever if secondary infectionis involved. Pressure threshold measurements with a thresholdmeter will indicate that discomfort occurs at a lower thresholdthan before the injury. Proximal to the injury, there may be acold spot caused by vasoconstriction, which may affect healing.

Initial therapy of the acute symptoms of myositis includes im-mediately applying ice to the affected structure to reduce swelling,limiting movement to within painless boundaries, and resting theaffected part. In injured mandibular muscles, restricting mouthopening during function and using a dental intraoral bite guardto control closure should be supported by NSADIs. In a severecase, immediately applying a methylprednisolone dose pack cancontrol the amount of the immediate swelling. Antibiotics canbe used if secondary infection is possible.

After the acute symptoms have subsided, treatment shouldinclude increased heat and mobilization of the affected structure,then an exercise program to regain full range of motion, andfinally a muscle strengthening program.

Fibrosis and Contracture. Myotatic contracture occurs in mus-cles that are not allowed to function within their full range ofmotion. The muscle will lose its stretch reflex capabilities andwill gradually shorten. Prolonged pain or immobilization can leadto myotatic contracture.113

Contracture can occur in the masticatory muscles if patientsare unwilling or unable to open their mouths fully. Patients oftenreport avoiding opening wide for fear of hearing clicking or crepi-tus, and others may not open wide because of past or present pain.Over time, this practice leads to the development of a habituatedprotective pattern, causing myotatic contracture. Likewise, re-stricted movement of the cervical region results in myotatic con-tracture.

Myofibrotic contracture often occurs as a result of infectionthat leads to fibrous changes in the muscle or its sheath. Traumato a muscle and the resultant inflammation and splinting maylead to fibrosis—an irreversible condition. Radiation therapy,incision through a muscle with fibrotic healing, and disuse forlong periods (more than 6 weeks) can also result in myofibroticcontracture.

In patients with masticatory muscle involvement, myotatic ormyofibrotic contracture will appear with limited interincisalopening. If the elevator muscles are involved, deviation will occur


on opening but not on protrusion. Lateral movement will benormal. Pain will not be present without sudden and forcefulstretching or biting.

The treatment for myotatic contracture is to gradually stretchthe involved muscle. Ultrasound with 5% to 10% hydrocortisonecream can be used as adjunct therapy. Massage and myofascialrelease along with daily stretching and exercise will bring themuscle slowly back to function. Myofibrotic contracture is irre-versible and requires surgical intervention for a patient whosefunction is severely impaired.

Muscle Disorders Secondary to Internal Derangement. In thepresence of acute or chronic internal derangement, the musclesthat support and move the joints can be secondarily affected.Splinting helps prevent further injury to the joint. In cases ofanterior disc displacement without reduction (closed lock), thejoint will often be immobile. The masticatory elevator musclesshould be splinted until the joint is healed.

The clinical finding of elevator spasm often causes the physi-cian or dentist unfamiliar with TMD to prescribe muscle relax-ants. These medications override the body’s defense mechanismsand so may do more harm than good. If the internal derangementis not adequately treated, the muscles remain chronically short-ened and may eventually undergo contracture. A patient withacute closed lock often presents with a history of joint clicking.The patient may or may not be able to pinpoint an eliciting event.Sometimes the patient wakes up with the jaw locked. Other times,it locks during chewing. The patient will often have loss of poste-rior support through tooth wear, tooth breakdown, or missingor poorly restored posterior teeth.

Closed lock may be accompanied by a change in occlusionresulting from disc displacement, accompanying spasm of thelateral pterygoid, or both. The occlusion may shift to the contra-lateral side with a corresponding posterior open bite developingon the ipsilateral side. The patient may attempt to position theposterior teeth into contact but is hampered by joint pain andthe lateral pterygoid, which pulls the mandible in the oppositeside.

After acute trauma, the occlusion settles back to its preinjuredstate once the TMJ inflammation has subsided. However, if thepatient has a parafunctional habit or has lost vertical dimension,the joint will continue to be unevenly loaded, and healing willbe delayed. In such instances, the joint may become chronicallyinflamed and the muscles of mastication may continue to be ina state of protective splinting, spasm, or both.

If a patient has a combination of acute trauma, loss of poste-rior teeth, and moderate-to-severe parafunction, anterior disc dis-placement with intermittent locking of the TMJ is likely. Patientsoften report histories of trauma that are followed by a variableperiod of clicking, progressively increasing in frequency and cul-minating in an abrupt disappearance and an inability to open themouth. Differential diagnosis of a patient who has limited mouthopening must include internal derangement, as well as muscletrauma.

Muscle Disorders Secondary to Cervical Spinal Dysfunction.Muscle disorders may occur secondary to rotations, fixations,fusions, or injury or locking of the facets of the cervical, thoracic,lumbar, and sacral vertebrae. The history, physical examination,and radiographic evaluation, often done in conjunction with aphysiatrist or orthopedist, will reflect the acuteness and severityof the vertebral problem.

Disc herniations can secondarily affect the cervical musclesthrough protective splinting, which can eventually lead to chronicpostural changes. Nerve impingement and nerve root injuries canalso affect muscle function. Commonly seen cervical problems inrelation to TMDs occur at the following cervical levels.

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Occiput-Atlas. A reduction in the space between the posteriorspine of the atlas and the base of the occiput, as reported byRocabado,147 may cause pain by compressing the suboccipitaltissues. The pain will be perceived as a headache starting fromthe back of the head.

Acute or long-standing trauma can shift the occiput-atlas rela-tionship and may lead to chronic tension in the suboccipital mus-cles with resulting fixation and irritation of the C1 and C2 nerves.The pain will be referred from the back of the head to the eye,along the side of the head, along the skin over the TMJ, anddown along the angle of the mandible, radiating into the neck.

Rotation of the atlas is commonly seen in patients with TMDsand may be linked to changes in occlusal patterns and instabilityof mandibular position.139,147 Osteoarthritic degeneration andligament and muscle injury also occur at this level in acceleration-deceleration injuries.

Atlas/Axis Level. Trauma to this level may disrupt the transverseligament holding the odontoid process of the axis against theanterior arch of the atlas, allowing forward subluxation or dislo-cation of the atlas on the axis. A disruption of the C1-C2 articula-tion may also result in excessive stretching or kinking of the verte-bral artery secondary to hypermobility. This may lead totemporary vertebrobasilar syndrome with symptoms of vertigo,nausea, tinnitus, and visual disturbances.

Cervical rotation will be reduced because 40% to 50% ofrotation occurs at the atlas-axis articulation.147 Pain also limitsmovement. Fractures are always to be considered in trauma tothis region.

C4, C5, and C6. The level of greatest instability against accelera-tion-deceleration forces appears to be in the C4 to C6 region,with C4-C5 being primarily affected in hyperextension and C5-C6 in hyperflexion. Trauma may be to the ligaments, discs, andvertebral bodies, depending on the direction and magnitude ofthe force.

The cervical curve can be affected, and the patient will oftenhave a compensatory forward head posture, further perpetuatingthe problem.

Cranial Neuralgias

Trigeminal NeuralgiaThe cranial neuralgias, particularly trigeminal neuralgia, affectthe face and have specific diagnostic criteria and treatment mo-dalities. These disorders are covered in Chapter 66.

Neuropathic Facial Pain (see Table 67.13)The International Association for the Study of Pain (IASP) definesneuropathic pain as ‘‘Pain initiated or caused by a primary lesionor dysfunction in the nervous system.’’148 Thus, neuropathic painresults from pathology in the peripheral or central nervous sys-tem.148 These disorders are particularly common in the head andneck, probably as a result of the dense and specialized sensoryinnervation of this region. Unfortunately, these disorders greatlyaffect the patient’s life by interfering with important functions,such as feeding and speech.

In the past, any facial pain disorder without a definable causewas considered to be an idiopathic, ‘‘atypical’’ facial pain syn-drome. Over the years, many inappropriate ‘‘descriptive’’ diag-noses were given to these disorders (atypical trigeminal neuralgia,atypical facial pain, atypical odontalgia, phantom tooth syn-drome, and so on.) Under the current IHS classification1 (seeTables 67.5 and 67.6), these disorders are considered ‘‘central’’causes for headache and facial pain and are classified as ‘‘persis-tent idiopathic facial pain’’ (category 13.18).1

AQ1

AQ1AQ1


Complex regional pain syndrome (CRPS), a form of neuro-pathic pain can occur in the face.149 CRPS is covered in detail inChapter 25. Likewise, postherpetic neuralgia commonly affectsthe face and is covered in detail in Chapter 27.

PSYCHOSOCIAL CONSIDERATIONS

Assessment

As with other chronic pain conditions, psychosocial factors ex-plain much of the variance in the outcome of persistent facial paindisorders. Affective and anxiety symptoms, especially emotionaltrauma, have been implicated in precipitating and maintainingchronic orofacial pain.150 Marked somatic overconcern or somat-ization disorder can also compromise treatment in these disor-ders. Similarly, chronic disability behavior further compromisesthe patient’s status.

It has become a minimum standard of care to address criticalpsychosocial factors within the diagnostic interview, as under-scored by the IASP Curricula on Pain for Dental Schools.151,152

Consistent with this attention, the Research Diagnostic Criteriaincludes a 31-item questionnaire addressing psychosocial andphysical domains of chronic TMD. Other validated self-reportfacial pain scales also address psychosocial issues, and their usewithin multidisciplinary facial pain facilities is common.153–155

Treatment

As in other areas of chronic pain management, behavioral inter-ventions have been a mainstay of treatment for persistent facialpain. Time-limited, structured relaxation training is as effectiveas conventional occlusal splint therapy for temporal joint dys-function and related chronic myofascial facial pain disorders.Combined treatment is even more effective and provides longerlasting effects.156 Similarly, improving cognitive coping skills re-duces pain and improves function.157 Behavioral interventionstarget reducing anxiety and improving perceived control overpain. Biofeedback-assisted relaxation can also be effective, per-haps more so in limited subpopulations.158–160 More intensive,interdisciplinary treatment is often indicated for patients with aconstellation of severe psychosocial and disability behaviors.

Cost-effective behavioral group programs have also been usedin the early stages of facial pain syndromes and have reducedpain and improved coping skills. Most recently, Stowell et al.161

compared a brief behavioral treatment program emphasizingearly intervention to a standard approach in patients with ‘‘acuteTMD’’ (pain of less than 6 months duration). One-year follow-up data revealed clinical improvement and substantially fewerjaw-related health care dollars for the early intervention program.Overall, conservative interdisciplinary treatment appears to havethe most promising results. Ideally, these programs will be imple-mented before the chronic concomitants of facial pain develop.

CONCLUSIONCraniocervical pain is a common clinical problem and often adiagnostic challenge. Given the complex anatomy of the regionand the numerous discrete syndromes, a multidisciplinary ap-proach is frequently indicated for evaluating difficult or refrac-tory cases.

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AUTHOR QUERIESAQ1–Please confirm cross reference.

AQ2–There was a comma here instead of a period. That suggeststo me that the last part of this sentence may be missing.Please complete the sentence.

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