Orofacial Pain—Part I

AACN Clinical IssuesVolume 16, Number 3, pp. 333–346C© 2005, AACN

Orofacial Pain—Part IAssessment and Management ofMusculoskeletal and Neuropathic Causes

Eleni Sarlani, DDS, PhD; Birute A. Balciunas, DDS, MSD;Edward G. Grace, DDS, MA

Orofacial pain is a common complaint,affecting the lives of millions of peoplearound the world. Chronic orofacial painoften constitutes a challenging diagnosticproblem that can be complicated bypsychosocial factors and typically requiresmultidisciplinary treatment approaches.The fundamental prerequisite forsuccessful management of orofacial painis an accurate diagnosis. Generating adifferential diagnosis, which will ultimatelylead to a definite diagnosis, requiresthorough knowledge of the diagnosticrange of orofacial pain. There is a vastarray of orofacial pain categoriesincluding: (1) musculoskeletal,(2) neuropathic, (3) vascular,(4) neurovascular, (5) idiopathic, (6) paincaused by local, distant, or systemicpathology, and (7) psychogenic. This

article presents the salient clinicalfeatures and the therapeutic approachesfor the various subtypes ofmusculoskeletal and neuropathic pain.Musculoskeletal pain is the mostprevalent orofacial pain, withtemporomandibular disorders andtension-type headache being the mainexamples. Neuropathic pain developssecondary to neural injury and/or irritationand can be distinguished into episodic,including trigeminal neuralgia andglossopharyngeal neuralgia, as well ascontinuous, such as herpetic andpostherpetic neuralgia, traumaticneuralgia, and Eagle’s syndrome.(KEYWORDS: Eagle’s syndrome,myofascial pain, postherpetic neuralgia,temporomandibular disorders, trigeminalneuralgia)

Pain is one of the main symptoms for whichpatients seek medical attention. Pain in theorofacial region, in particular, can be verydistressing for the patient, since it usually af-fects important daily living functions, suchas chewing, swallowing, talking, and laugh-ing. Temporomandibular disorders constitutethe second most common cause of orofacialpain, following dental pain.1 There is a widevariety of additional conditions that should

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From the Department of Diagnostic Sciences andPathology (Drs Sarlani and Balciunas) and the De-partment of Health Promotion and Policy (Dr Grace),Brotman Facial Pain Center, Dental School, University ofMaryland, Baltimore.

Reprint requests to Eleni Sarlani, Assistant Profes-sor, Brotman Facial Pain Center, Dental School, Univer-sity of Maryland, 666 W. Baltimore Street, Room 2-A-15,Baltimore, MD 21201–1586 ([email protected]).

333

334 � SARLANI ET AL AACN Clinical Issues

be included in the differential diagnosisof the patient who presents with pain inthe orofacial region (Box 1). Notably, re-ferred pain is common in the orofacial struc-tures, representing a challenging diagnosticproblem.

A thorough history and examination is ofparamount importance in arriving at an ac-curate diagnosis. The evaluation of the pa-

BOX 1 � Classification of OrofacialPain

Musculoskeletal

1. Temporomandibular disordersa. Masticatory muscle disorders

• Myofascial pain• Myositis• Myospasm• Local myalgia

b. Articular disc derangements• Disc displacement with reduction• Disc displacement without reduction

c. Temporomandibular joint disorders• Synovitis/capsulitis• Osteoarthritis

2. Tension-type headache

Neuropathic

1. Episodica. Trigeminal neuralgiab. Glossopharyngeal neuralgia

2. Continuousa. Herpetic neuralgiab. Postherpetic neuralgiac. Traumatic neuralgiad. Eagle’s syndrome

Vascular

1. Giant cell arteritis2. Carotid artery dissection

Neurovascular

1. Migraine2. Cluster headache3. Chronic paroxysmal hemicrania

Idiopathic

1. Atypical facial pain2. Atypical odontalgia3. Burning mouth syndrome

Other diseases that can cause facial pain

1. Local pathology2. Distant pathology (referred pain)3. Systemic diseases

Psychogenic

1. Somatoform disorders2. Factitious disorders3. Malingering

tient begins with a medical history, includ-ing history of trauma to the head and neck,significant illnesses, current medications, andcomplete review of systems, with special at-tention to systemic disorders that can causefacial pain.2 A detailed description of the paincomplaint in terms of pain duration, loca-tion, intensity, quality, frequency, and pro-gression of pain since onset is an absoluteprerequisite for an accurate diagnosis.3 As-sociated symptoms that may accompany thefacial pain, as well as aggravating and al-leviating factors, can provide valuable di-agnostic information. A brief psychologicalscreening should be part of the history forall chronic pain patients, since depressionand anxiety are very common among thispatient population.4,5 Psychological distressmay be a contributing factor to the onset ormaintenance of pain, a consequence of pain,or a coexistent problem with independentetiology.

The clinical examination of the orofa-cial pain patient includes assessment of cra-nial nerve function, cervical spine evalua-tion (posture and range of motion), palpationof masticatory and neck muscles, temporo-mandibular joint examination (tenderness topalpation, range of motion, joint sounds),and complete intra-oral and dental evalua-tion. Depending upon the findings of thehistory and clinical evaluation, appropriatelaboratory tests and diagnostic imaging pro-cedures may be required.

Orofacial pain can be classified into:(1) musculoskeletal, (2) neuropathic, (3) vas-cular, (4) neurovascular, (5) idiopathic, (6)pain caused by local, distant, or systemicpathology, and (7) psychogenic (Table 1).This article elaborates on the differential di-agnosis and management of musculoskele-tal and neuropathic orofacial pain. Tem-poromandibular disorders and tension-typeheadache constitute the main subcategoriesof musculoskeletal facial pain. Neuropathicorofacial pain is subdivided into episodic,including trigeminal and glossopharyngealneuralgia, as well as continuous, such as her-petic and postherpetic neuralgia, traumaticneuralgia, and Eagle’s syndrome. A compre-hensive reference section has been includedfor those who wish to gain further informa-tion on a particular entity; many additional

Vol. 16, No. 3, July-Sept 2005 OROFACIAL PAIN—PART I � 335

Figure 1. Temporomandibular joint anatomy. The capsule has been cut away to reveal the disc and its relationshipto the articulating surfaces of the joint. Reprinted with permission from Hiatt JL, Gartner LP. Textbook of Head andNeck Anatomy, Ed. 1. Baltimore, Md: Williams & Wilkins; 1987.

figures and diagrams can be found in the var-ious textbooks that are cited.

� Musculoskeletal Pain

Temporomandibular Disorders

Temporomandibular disorders (TMD) is acollective term referring to a variety of patho-logic conditions that affect the masticatorymusculature, the temporomandibular joints(TMJ) or both (see Figure 1). The clinicalpresentation is variable and can include fa-cial pain that is aggravated by jaw function,tenderness upon joint and muscle palpation,limited mandibular range of motion, devia-tion or deflection of the mandible on mouthopening, and TMJ sounds.6,7 Occasionally,patients may also complain of tinnitus, ear-aches, headaches, and dizziness. Signs andsymptoms of TMD are very prevalent amongthe general population. It is estimated that40% to 75% of nonpatient adults have at least

one sign, and 33% at least one symptom ofTMD.6 Temporomandibular joint sounds arevery common, presenting in approximately30% of the general population, but they arenot considered a specific indicator of pain-related pathology, and they do not warranttreatment when no other symptoms or signsare present.8

Temporomandibular disorders constitutethe most common cause of chronic painin the orofacial region. Approximately 12%of the general population is affected by TMD,and 5% of the population has symptomssevere enough to warrant treatment.1,7 Theincidence of new onset TMD pain rangesbetween 1.6% to 3.9% per year.9 Temporo-mandibular disorders are more prevalentamong women, with a female-to-malegender ratio of 2:1.9 Women-to-men ratio isestimated to be 8:1 among individuals seek-ing treatment for TMD.10 Greater willingnessof women to report pain may play a role inthe highly disproportionate representation of


the two sexes among clinical TMD cases.11

In addition, pain severity and persistenceare major predictors of use of healthcare,suggesting that women experience pain ofgreater average severity than men.12 Genderis also a significant predictor of chronicityamong patients who present with acuteTMD.8 Garofalo et al13 reported that femalespresenting with acute TMD were significantlymore likely to report pain at 6-month followup compared to male patients.

Putative etiological and/or contributoryfactors include trauma involving local tis-sues, repetitive chronic microtrauma (eg,teeth grinding or clenching), unaccustomedjaw use (eg, opening the mouth wide for along dental appointment), genetic vulnerabil-ity, increased level of emotional stress, poorsleep, and occlusal disharmony.7,14–18 Tem-poromandibular dysfunction has also beenreported secondary to orotracheal intuba-tion or endoscopy.19,20 Moreover, hyperex-citability of the central nervous system no-ciceptive pathways as well as dysfunctionof the endogenous pain inhibitory systemshave also been implicated in the develop-ment and/or maintenance of TMD-relatedchronic pain.21–23 Overall, the current knowl-edge suggests that TMD have a multifactorialorigin, which might benefit from a multidis-ciplinary management.

Temporomandibular disorders are classi-fied into 3 main categories: (1) masticatorymuscle disorders, (2) articular disc de-rangements, and (3) temporomandibularjoint disorders. The most common types ofthese TMD categories are described in thefollowing text.

MASTICATORY MUSCLE DISORDERS: Accordingto the American Academy of OrofacialPain,6 masticatory muscle disorders can bedivided into 4 subtypes: (1) myofascial pain,(2) myositis, (3) myospasm, and (4) localmyalgia.

Myofascial Pain: Myofascial pain is character-ized by the presence of focal, exquisitelytender muscle areas, called trigger points.Trigger points are typically found in taut mus-cle bands and produce a characteristic painreferral pattern on palpation.24,25 The patientcomplains of constant, dull muscle pain thatis typically exacerbated by muscle use.6 Fre-

quently, the referred pain is the only symp-tom and the patient is unaware of the triggerpoints.26 Trigger points in the masseter andtemporalis muscles can refer pain to poste-rior teeth, while trigger points in the stern-ocleidomastoid and trapezius muscles oftenrefer pain to the jaw or temple (Figure 2).3,25

Accordingly, the condition may present as

Figure 2. Pattern of pain referral and location (X) ofa trigger point (TrP1) in the upper trapezius muscle.Reprinted with permission from Simons DG, Travell JG,Simons LS. Travell and Simons’ Myofascial Pain andDysfunction: The Trigger Point Manual, Vol. 1—UpperHalf of Body, Ed. 2. Baltimore, Md: Lippincott Williams& Wilkins; 1999.


toothache or headache and careful palpationof the head and neck muscles is required toreveal the trigger points. Palpation of the trig-ger points will elicit severe local pain, as wellas aggravation of the referred pain. Replica-tion of the patient’s symptoms upon triggerpoint palpation will confirm the diagnosis.

Teeth clenching, trauma, somatization,and psychological distress have been iden-tified as contributing factors for the devel-opment of chronic masticatory myofascialpain.14,16 In addition, Velly et al16 reported thatthe risk of myofascial pain was 3 times higherin women compared to men. Sleep distur-bances, central nervous system dysfunction,nutritional deficiencies, or fatigue may alsoplay a role in the etiopathogenesis of thiscondition.6,24 Treatment is aimed at elimina-tion of precipitating factors and inactivationof trigger points by vapocoolant spray orinjection of a local anesthetic, followed bystretching.27 Relaxation therapy, daily stretch-ing of the affected muscles, physical therapymodalities, and medications, such as anal-gesics, muscle relaxants, and tricyclic antide-pressants in low doses can also be helpful.26

Myositis: Myositis refers to true muscle inflam-mation and is an uncommon cause of oro-facial pain that may result from a spread-ing infection or acute trauma to the muscletissue.6 This condition is easy to diagnose,since it presents with the cardinal signs ofinflammation; there is constant pain as wellas swelling, erythema, and elevated temper-ature over the affected muscle.6 Pain uponpalpation as well as limitation of mandibularrange of motion secondary to pain are alsoapparent. Treatment of the underlying infec-tion with antibiotics is required. In the case ofmuscle injury, rest should be advised in theearly posttraumatic phase to limit hematomaformation.28 Supporting therapy may con-sist of ice and nonsteroidal anti-inflammatorydrugs (NSAIDs).

Myospasm: True myospasm is uncommonamong TMD patients. Myospasm is an acutecondition, characterized by severe musclepain, marked limitation of mouth openingand, often, acute malocclusion.6 There is asignificant increase in electromyographic ac-tivity, secondary to sustained, involuntarymuscle contraction.6 Treatment is aimed at

stretching the muscle to full length; thiscan be achieved only after reducing thepain by ice, vapocoolant spray, or injectionof local anesthetic.7 Injections of botulinumtoxin are recommended for severe and recur-rent myospasms.29 In such cases, predispos-ing factors, including psychological distressand parafunctional activities, also should beaddressed.

Local Myalgia: The term local myalgia wasadopted by the American Academy ofOrofacial Pain to denote muscle pain con-ditions that cannot be attributed to a spe-cific cause, such as trigger points, inflam-mation, or muscle spasm.6 Local myalgiais a common temporomandibular disorderthat is characterized by spontaneous mus-cle pain, muscle tenderness upon palpation,as well as limited mouth opening due tothe pain.6 Typically, the symptoms are ag-gravated by activities requiring jaw move-ment, such as chewing, talking, laughing,or yawning. Treatment approaches includepatient education on painless use of themandible, moist heat applications, jaw exer-cises, and short-term use of NSAIDs or mus-cle relaxants.30,31 An intraoral stabilizationappliance may be of benefit if jaw para-functional activities are suspected, while re-laxation therapy can be recommended forpatients that report high stress levels.32 Train-ing in diaphragmatic breathing, postural re-laxation, improvement of sleep patterns, andphysical activity have also been shown to beeffective in reducing the symptoms.33

ARTICULAR DISC DERANGEMENTS: Articular discderangements are usually characterized bydisplacement of the articular disc anteriorlyand medially. Alterations in the disc-condylestructural relation may result from elongationof the discal ligaments, secondary to trauma.7

High levels of anxiety and clenching andgrinding of the teeth have also been impli-cated as risk factors.34

Disc Displacement With Reduction: Disc displace-ment with reduction is characterized by im-provement of the position of the displaceddisc during opening. An opening joint click-ing occurs as the condyle positions itselfunder the posterior band of the disc uponmouth opening, and a closing joint clickingcan be heard as the condyle slips off the


disc, just before the teeth come together.7

The patient may complain of episodic andmomentary catching of the jaw movementduring mouth opening. Pain may or may notbe present.6 Asymptomatic clicking is a verycommon sign among the general populationand does not require treatment; however, pa-tients should be counseled as to the natureof the clicking.35

Disc Displacement Without Reduction: Disc displace-ment without reduction refers to an altereddisc-condyle structural relation that is not im-proved during mouth opening. Frequently,there is a history of clicking and sudden onsetof hypomobility. The displaced disc blocksthe condylar movement, resulting in limited(25 to 30 mm) mouth opening and restrictedlateral excursion to the contralateral side.7

The mandible deflects to the affected sideon opening and clicking noises are absent.6,7

Pain is typically present in the acute con-dition, while chronic disc dislocation maybe nonpainful. With the progression of thecondition, there is a gradual increase in themandibular range of motion.6,7 Milano et al36

reported an association between nonreduc-ing disc displacement and structural bone le-sions, suggesting that disc displacement with-out reduction can predispose to the onsetof osteoarthritis. When a patient with limitedmouth opening requires tracheal intubation,fibreoptic intubation is indicated, since op-timal visualization of the larynx cannot beachieved by direct laryngoscopy.37

Magnetic resonance imaging can be usedto substantiate the clinical diagnosis andrule out other pathological conditions ofthe TMJ that would result in blockageof condylar movement.38–40 In acute discdislocation, there should be an effort toreduce the disc dislocation by manual ma-nipulation, followed by insertion of an an-terior repositioning appliance.7 Managementof chronic disc dislocation may include a sta-bilization appliance, physical therapy, andNSAIDs if pain is present.7 Surgical arthro-centesis or arthroscopy may be beneficial forpatients who are refractory to conservativetreatment.41,42

TEMPOROMANDIBULAR JOINT DISORDERS

Synovitis and Capsulitis: Synovitis and capsulitisare characterized by inflammation of the syn-

ovial lining of the TMJ and the capsular lig-ament respectively. They are grouped to-gether since they cannot be distinguishedon the basis of historical or clinical findings.Synovitis and capsulitis are characterized byconstant deep pain in the TMJ, tenderness toTMJ palpation, and restricted mouth openingsecondary to pain; acute malocclusion of theposterior teeth on the affected side may alsobe present.6 Nishimura et al43 found a pos-itive correlation between the concentrationsof bradykinin in synovial fluid and the degreeof arthroscopically-assessed synovitis.

Synovitis and capsulitis can be induced bytrauma to the jaw or repetitive chronic mi-crotrauma. In the case of acute trauma, iceshould be applied to the affected joint 4 to6 times daily for the first 24 to 36 hours, fol-lowed by moist heat applications for 10 to 15minutes, 3 to 4 times per day. Restriction ofjaw movement to a pain free range of motionand administration of NSAIDs on a regularbasis for 10 to 14 days are recommended.7 Astabilization appliance can be of benefit, es-pecially if parafunctional habits are present.

Osteoarthritis: Osteoarthritis is a non-inflammatory arthritic condition charac-terized by deterioration of the articularsurfaces. It presents with pain that is exacer-bated by mandibular movement, tendernessupon palpation of the joint, crepitus, andlimited range of mandibular motion.6,7 Theclinical diagnosis is substantiated by radio-graphic and magnetic resonance imagingevidence of structural bony changes, suchas surface irregularities, flattening or erosionof the condyle, and osteophytes.40,44 Conser-vative approaches including NSAIDs, moistheat applications, painless use of mandible,jaw exercises and stabilization applianceconstitute the mainstay of treatment.7,45

For refractory cases, one or two singleinjections of corticosteroids in the joint,arthrocentesis, or arthroscopic surgery maybe recommended.46,47

Tension-type Headache

Episodic tension-type headache (ETTH) is acommon primary headache affecting the oc-cipital, parietal, temporal, or frontal areas. Ac-cording to the second edition of The Interna-tional Classification of Headache Disorders,48

infrequent ETTH refers to < 12 headache days


per year, while frequent ETTH to ≥1 but < 15headache days per month. The pain is typ-ically bilateral, has a tightening or pressingquality, mild to moderate intensity, and maylast from a few hours to 7 days.48,49 In con-trast to migraine, there is no nausea, vom-iting, or aggravation of the pain by routinephysical activity. However, anorexia may ac-company the pain, and occurrence of eitherphotophobia (sensitivity to light) or phono-phobia (sensitivity to sound) does not ex-clude the diagnosis. The pain may be precip-itated by stress and is usually associated withfatigue and poor sleep. Treatment consists ofstress management, relaxation training, andpharmacotherapy.49 Simple analgesics andNSAIDs are typically effective in aborting thepain.50

Chronic tension-type headache (CTTH)has characteristics similar to ETTH, butis characterized by presence of headacheon ≥15 days per month for at least 3months. Chronic tension-type headache usu-ally evolves from ETTH and may be asso-ciated with no more than one of the fol-lowing: photophobia, phonophobia, or mildnausea. Even though CTTH is often refrac-tory to treatment, stress management, physi-cal therapy, and prophylactic pharmacother-apy with tricyclic antidepressants may bebeneficial.50–52

The pathophysiology of tension-typeheadache is elusive. The present review, forclassification purposes, categorizes tension-type headache in the group of musculoskele-tal disorders; however, it has been hypoth-esized that there is a continuum betweentension-type headache and migraine.53 Sen-sitization of the nociceptive central nervoussystem pathways secondary to nitric oxideproduction, has also been implicated; in-hibition of nitric oxide was found effec-tive in CTTH, providing hope for morespecific and successful treatment in thefuture.50,52,54

Chronic tension-type headache needs tobe differentiated from medication overuseheadache, which is the result of fre-quent use of anti-headache drugs (anal-gesics, ergot alkaloids, serotonin agonists,combined preparations with caffeine orcodeine).55 Withdrawal therapy, often un-der in-patient conditions, is essential for theeffective management of medication overuseheadache.55

� Neuropathic Pain

Episodic Neuropathic Painhe

TRIGEMINAL NEURALGIA: Trigeminal neuralgia(TN) is an uncommon facial pain condition,characterized by episodic, lancinating painin the distribution of one or more divisionsof the trigeminal nerve.56 The pain may beaccompanied by a contraction of the facialmusculature (hence the term tic douloureux).The disorder is more prevalent between thefifth and seventh decade; it has a female pre-ponderance (female to male gender ratio of1.74:1) and an annual occurrence rate of 4–5 per 100,000 population. Trigeminal neu-ralgia is typically unilateral (96% of cases)and affects most commonly the maxillary ormandibular division.

The pain is described as severe, electric-shock like, and lasts only for seconds; the pa-tient is typically asymptomatic between thepain attacks. The pain paroxysms are of-ten evoked by nonnoxious stimulation, suchas light touch or vibration, to trigger areasextraorally and/or intraorally.56 The triggerzones are localized on the affected side, butthey do not always coincide with the areaof pain. Common extraoral trigger zones oc-cur above the supraorbital foramen, the innercanthus of the eye, lateral to the ala nasi, andover the mental foramen. Typically, immedi-ately following a jab of pain, there is a re-fractory period during which further pain at-tacks cannot be evoked. Trigeminal neuralgiais characterized by spontaneous remissionsthat may last months or even years. Neverthe-less, with time, pain attacks become more fre-quent, while remissions occur less often andlast for a shorter time period.57 In prolongedcases, patients may develop atypical features,such as persistent pain between episodes.57

The intermittent temporal pattern and thesevere intensity of TN resemble those of clus-ter headache or chronic paroxysmal hemi-crania. However, the pain attacks of clusterheadache and chronic paroxysmal hemicra-nia cannot be triggered by light touch, havea longer duration, and awaken the patientfrom sleep. Moreover, these headache disor-ders occur typically between the third andfourth decade of life and are accompaniedby ipsilateral autonomic phenomena. Occa-sionally, the paroxysmal pain of TN affectsthe dentition and can confused with dental


pain.58 In these cases, the patient often un-dergoes multiple invasive dental proceduresbefore the correct diagnosis is reached. Fail-ure of dental treatment to provide long-termpain relief should raise the suspicion of TN.An important feature that distinguishes TNfrom dental pain is that TN typically does notinterrupt the patient’s sleep. Moreover, painoriginating from dental pathology is usuallyprogressive and its character changes withtime.59 Tooth vitality tests and radiographicexamination will also serve to exclude den-tal pathology.

Trigeminal neuralgia may develop sec-ondary to posterior fossa compressive le-sions; intracranial tumors are detected in2% of patients who present with typicalTN.60 Trigeminal neuralgia may also be in-duced by demyelinating plaques of multi-ple sclerosis involving the trigeminal noci-ceptive pathway.61,62 Thorough medical andneurological examinations as well as imag-ing are required to rule out such underlyingconditions. Occasionally, neurological signsindicative of secondary causes of TN be-come apparent only later in the course ofthe disease, emphasizing the importance ofrepeating neurological examinations in TNpatients.62,63

Idiopathic TN is thought to be induced byvascular compression of the trigeminal root-entry zone, which results in demyelinationof trigeminal sensory fibers.64,65 Histopatho-logical examination of trigeminal nerve rootsfrom patients with compression of the nerveroot by a blood vessel reveals focal lossof myelin, close apposition of the demyeli-nated axons, and lack of intervening astro-cytic processes.64 Demyelination may resultin ectopic generation of action potentials,presenting clinically as spontaneous pain,while ephaptic neural transmission may un-derlie the generation of pain by innocu-ous stimulation.66 Over the course of time,excessive afferent input of nerve impulsesmay produce central sensitization, resultingin atypical TN features, such as constantpain.57,67

Pharmacological therapy is the firstline of treatment for TN; the goal is thereduction of neuronal hyperexcitability inthe peripheral and/or the central nervoussystem.68 Carbamazepine is the mainstay ofpharmacotherapy of trigeminal neuralgia.69

Additional potentially effective medica-tions include oxcarbazepine, lamotrigine,phenytoin, gabapentin, and tizanidine.69–71

Often drug combinations are used tomaximize effectiveness and minimize ad-verse effects.72 Surgical intervention isrecommended if pharmacological treatmentbecomes ineffective or adverse effectsbecome intolerable. Microvascular decom-pression of vessels compressing the nerveroot is very effective and has low incidenceof recurrence.73,74 However, it entails poste-rior fossa craniotomy and involves seriousrisks, such as hearing impairment, ataxia,brain stem infarction, cerebellar injury, anddeath.74 Percutaneous ablative techniquesinvolve lesioning at the level of the gasserianganglion by percutaneous radio-frequencythermocoagulation, injection of glycerol, orballoon compression.75–77 These procedureshave good initial results and carry less riskthan microvascular decompression; however,they are associated with a higher incidenceof pain recurrence. Potential complicationsinclude loss of touch sensation, dysesthesias,and anesthesia dolorosa. Gamma knifesurgery involves lesioning of the trigeminalnerve at the root entry zone using stereotac-tic techniques and radiation between 70 and90 Gy.78,79 This procedure is less invasive andthus suitable for medically compromised pa-tients. Outcomes are similar to other ablativeprocedures.80–82 Facial sensory loss, paresthe-sias, and dysesthesias are the most commoncomplications.77,78

GLOSSOPHARYNGEAL NEURALGIA: Glossopharyn-geal neuralgia is a rare pain condition that issimilar to trigeminal neuralgia but it involvesthe distribution of the glossopharyngealnerve. It has a prevalence of approximately0.2% to 1.3% of that of TN and is more com-mon in the sixth through eighth decades.83

Glossopharyngeal neuralgia is characterizedby severe, sudden, unilateral, stabbing painin the ear, base of the tongue, tonsillar fossa,or beneath the angle of the mandible.84 Paintypically lasts a few seconds to 2 minutes andcan be triggered by swallowing, chewing,talking, coughing, or yawning.83 Frequently,patients experience remission of pain lastingmonths to years. Pharmacological treatmentis the same as for TN. In patients with medi-cally intractable glossopharyngeal neuralgia,


surgical treatment may alleviate the symp-toms. This involves either intracranial sectionof the 9th nerve and the upper two rootlets ofthe 10th nerve, or microvascular decompres-sion. Microvascular decompression of theglossopharyngeal nerve has been shown tobe a long-term effective procedure with min-imal complications, mainly hoarseness anddysphagia.84,85

Continuous Neuropathic Pain

HERPETIC AND POSTHERPETIC NEURALGIA: Follow-ing a chickenpox infection, the varicella-zoster virus becomes latent in the cranialnerve and dorsal root ganglia. Reactivationof the virus later in life can result in her-pes zoster, which is characterized by vesci-cular eruption and associated severe painin the distribution of the affected branch.Often, prodromal symptoms, such as pain,itching, and malaise precede the rash.86

Herpes zoster disproportionately affects theimmune-compromised as well as the el-derly, possibly due to an age-related declinein varicella-zoster virus-specific, T-cell medi-ated immunity.86,87 The trigeminal ganglion isinvolved in approximately 10% of cases, withthe ophthalmic division being most com-monly affected. Antiviral drugs and systemiccorticosteroids are the mainstreams of treat-ment; opioids may also be required to controlthe severe pain that accompanies the herpeticrash.86

Pain that persists longer than 3 to 4 monthsfollowing the outbreak of herpes zoster erup-tion is referred to as posteherpetic neural-gia. Posteherpetic neuralgia affects 5% to20% of herpes zoster patients, mainly el-derly individuals.88,89 Additional risk factorsfor the development of persistent pain fol-lowing a herpes zoster infection include fe-male gender, prodromal pain, adverse psy-chosocial factors, as well as greater rashseverity and higher acute pain intensity.86,88,90

Postherpetic neuralgia presents as con-tinuous severe, burning pain with sharpexacerbations. Tactile allodynia (pain in re-sponse to an innocuous stimulus) and hy-peralgesia (exaggerated pain in response toa noxious stimulus) are often present, com-promising significantly the patient’s quality oflife. Since no apparent peripheral pathologyis evident upon clinical examination, careful

questioning is needed to rule out a history ofvesicular/ulcerative lesions, which wouldlead to a definite diagnosis.

Medications that have been proven effec-tive in controlled clinical trials include thelidocaine patch 5%, gabapentin, tricyclic an-tidepressants, and opioids.91,92 Topical cap-saicin may also be helpful, but it is poorlytolerated.86 Frequently, a combination of var-ious medications is necessary in order to ob-tain adequate pain control.91 Bowsher et al93

reported that tricyclic antidepressants treat-ment is more efficacious when initiated earlyin the course of the disease. Postherpeticneuralgia is often refractory to treatment.Thus, emphasis is placed on its prevention.Administration of antiviral agents during theherpetic rash not only attenuates the severityof the acute infection, but also significantlyreduces the risk of chronic pain.89,94 In ad-dition, recent animal studies suggest that ad-ministration of gabapentin can alleviate theherpes zoster pain, as well as reduce the inci-dence of postherpetic neuralgia.95 These find-ings, however, remain to be tested in humansubjects.

TRAUMATIC NEURALGIA: Traumatic neuralgia oc-curs following direct neural injury and deaf-ferentation. Occasionally, there is a delay inthe onset of pain after the initial injury.96 Thepain is typically described as constant andburning, while superimposed lancinating ex-acerbations may also occur.96 Abnormal sen-sations, such as allodynia and hyperalgesia,and neural sensory or motor deficits oftenaccompany the pain.3 Pharmacological man-agement consists of tricyclic antidepressants;administration of anticonvulsant medications,such as carbamazepine or gabapentin, is alsoadvocated if there are sharp, shooting qual-ities to the pain.97 Topical applications ofcapsaicin may desensitize the affected areaand alleviate the symptoms, while sparingthe patient of the adverse effects of systemicdrugs.3,98

EAGLE’S SYNDROME: Eagle’s syndrome is an un-common condition resulting from compres-sion of the glossopharyngeal nerve by anelongated styloid process or an ossified stylo-hyoid ligament. The condition is more preva-lent among females.99,100 The chief signs andsymptoms include dull and persistent neck


and throat pain, dysphagia, otalgia, and aforeign body sensation.99–101 Radiation of thepain to the TMJ or the upper limb has alsobeen reported.100 The pain may have a neu-ralgic component, mimicking glossopharyn-geal neuralgia, and it is usually exacerbatedby rotation of the head to the contralat-eral side, swallowing, extending the tongue,and yawning.101 It is suggested that abnor-mal bone formation, leading to an elon-gated styloid process or an ossified stylohy-oid, may be secondary to soft tissue injury,such as tonsillectomy.102 However, most pa-tients report no previous history of trauma ortonsillectomy.100

Plain radiographs and computed tomogra-phy examination will reveal elongation of thestyloid process or ossification of the stylohy-oid ligament.101,103 Elongation of the styloidprocess occurs in approximately 4% to 28%of the general population; however, in mostcases it is asymptomatic.102,103 In addition,patients with bilateral elongation frequentlycomplain of unilateral neck pain. Therefore,establishment of the diagnosis is greatly fa-cilitated by replication of the patient’s symp-toms on palpation of the tonsillar fossa, aswell as alleviation of the pain by injection oflocal anesthetic.100,103 Surgical resection of thestyloid process or the calcified stylohyoid lig-ament, through an intraoral or extraoral ap-proach, results in resolution of the symptomsin most patients.99,100,103,104 Concurrent treat-ment with NSAIDs is advocated, in order toprevent re-ossification following the surgicalprocedure.102

� Summary

Musculoskeletal pain, including temporo-mandibular disorders and tension-typeheadache, is very common among orofacialpain patients. Temporomandibular disorderscan be subdivided into various muscle,articular disc, and joint pathoses, whichpresent with different clinical characteristicsand require diverse treatment. Conservative,reversible approaches are recommendedas the first line of treatment. Arthrocentesisand arthroscopy may be indicated for discand joint conditions that are refractory toconservative therapy, but are not beneficialfor muscle disorders.

Neuropathic pain occurs following neuralinjury or irritation and can be distinguished asepisodic or continuous. Trigeminal and glos-sopharyngeal neuralgia constitute the mainexamples of episodic neuropathic pain. Theunique clinical characteristics of these disor-ders, including their temporal pattern, dis-tinct distribution, and nonnoxious triggeringof the pain, greatly facilitate the diagnosis.Continuous neuropathic pain, such as pos-therpetic and traumatic neuralgia, is often de-scribed as burning, may be accompanied byallodynia and hyperalgesia, and can be resis-tant to various treatment approaches.

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Orofacial Pain—Part I