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Orofacial pain
C H A P T E R
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Orofacial Pain Jason E. Pope, MD b Samer Narouze, MD, MSc, DABPM, FIPP
The incidence and prevalence of orofacial pain in the general population is very high. Care and emphasis should be placed on correct diagnosis and treatment rather than on symptomatic management. Each disorder will be described according to the classification and diagnostic criteria published in the International Classification of Headache Disorders, second edition (ICHD-2). The pathophysiology of the disorder, the clinical picture, and the management (both medical and interventional if applicable) will be reviewed. The ICHD-2 criteria provide a systematic classification for headache and orofacial pain and are divided into three parts: the primary headaches, the secondary headaches, and cranial neuralgias central and primary facial pain.1 We will focus mainly on Sections 11 and 13 of the ICHD-2 (Table 42-1). However, before considering the diagnoses that are commonly attributed to orofacial pain, it is relevant to provide a brief comment on eliciting the key components of the history and physical examination in the evaluation of headache and orofacial pain. It is important to take a stepwise, systematic approach to the patients pain. This requires a fundamental knowledge of the ICHD-2 criteria. It should be noted that in one series of 97 consecutive patients presenting to a tertiary care neurologic facility, 29% were not classifiable using the ICHD-2 criteria.2 An appropriate physical examination includes a thorough neurologic assessment (including gait, pronator drift, Romberg’s sign, and reflex testing, that is, Hoffman and Babinski signs), heart and carotid auscultation, fundoscopic examination, cervical range of motion (ROM including atlantoaxial and atlantoocciptial joint), a musculoskeletal evaluation with careful detail to myofascial tenderness and trigger points, maneuvers that provoke radicular signs (Spurling’s test), cervical facet examination, and Waddell’s signs of nonorganic pain (tenderness to palpation, stimulation, distraction, regional disturbance in function, and overreaction). Tables 42-2 and 42-3 list findings and characteristics indicating the need for neuroimaging evaluation, respectively.3
ANATOMY AND PATHOPHYSIOLOGY The trigeminal system provides the relay system for pain and touch sensation to the face, as well as motor function to the muscles of mastication. The trigeminal system is a bilateral structure that spans from the midbrain to the medulla and is composed of four nuclei: the mesencephalic nucleus, the main sensory nucleus, a spinal nucleus of V, and the motor nucleus. The caudal portion of the trigeminal system nucleus is referred to as the spinal nucleus of V and is composed of three regions, in cephalad to caudal order, the subnucleus oralis, the subnucleus interplaris, and the subnucleus caudalis. The subnucleus caudalis is very similar in structure and function to the dorsal horn and extends down to the second or third cervical © Copyright 2011 Elsevier Inc., Ltd., BV. All rights reserved.
level. The primary afferent synapses ipsilaterally in the nucleus caudalis and then the second-order neuron crosses to join the contralateral spinothalamic tract. The trigeminal pathway is termed the ventral trigeminothalamic tract and terminates in the ventral posteromedial (VPM) nucleus of the thalamus. Activation of nuclei in close proximity to the trigeminocervical complex may explain the associated aura and symptoms attributed to different headache disorders by either activation of wide dynamic neurons, ephaptic transmission, or by sheer close proximity to the complex (solitary nucleus, nucleus ambiguous, or dorsal nucleus of vagus nerve). Goadsby demonstrated the trigeminocervical convergence mechanism (Fig. 42-1). He electrically stimulated the superior sagittal sinus of adult monkeys and C-fos was expressed in the superficial laminae of the dorsal horn of C1 and C2, but none in C3.4 Anthony examined patients with occipital headache and he summarized that “projection of pain . . . overlap between trigeminal nucleus and upper cervical cord . . . form a column of cells forming the posterior horn . . . to C4.”5 Consequently, the trigeminocervical complex with the hypothesized reciprocal interactions described by Goadsby, appear to introduce potential neuromudulatory/ablative sites for a variety of headache disorders, contrary to the accepted headache generator foci.
HEADACHE ATTRIBUTED TO DISORDER OF CRANIAL BONE The diagnostic criteria include pain in one or more regions in the head and face with clinical, laboratory, or imaging evidence of a lesion within the cranial bone known to be valid evidence of generating headache (Table 42-4). The source of the pain must be in close temporal association to and is maximal over the bone lesion, and with resolution of the pain after successful treatment of the bone lesion. Most disorders of the skull are not painful, with the exception of osteomyelitis, multiple myeloma, and Paget’s disease.
HEADACHE ATTRIBUTED TO DISORDER OF NECK These constellations of disorders involve pain referral from neck structures to the head/and or face. The diagnostic criteria hinges on what is excepted as “being generally accepted as valid cause of headache.”
CERVICOGENIC HEADACHE Cervicogenic headache is pain attributed to a disorder or lesion within the cervical spine or soft tissues that is generally accepted to cause headache or facial pain. (Please refer to Chapter 41). 283
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TABLE 42–1 ICHD-2 Classification Headings
Part I: The Primary Headaches 1. Migraine 2. Tension-type headache 3. Cluster headache and other trigeminal autonomic cephalalgias 4. Other primary headaches Part II: The Secondary Headaches 5. Headache attributed to head and/or neck trauma 6. Headache attributed to cranial or cervical vascular disorder 7. Headache attributed to nonvascular intracranial disorder 8. Headache attributed to a substance or its withdrawal 9. Headache attributed to infection 10. Headache attributed to disorder of homoeostasis 11. Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cranial structures 12. Headache attributed to psychiatric disorder Part III: Cranial Neuralgias Central and Primary Facial Pain and Other Headaches 13. Cranial neuralgias and central causes of facial pain 14. Other headache, cranial neuralgia, central or primary facial pain
TABLE 42–2 Headache with “Red Flag” Symptoms and Signs That Require Further Work-up
Sudden onset of headache (thunderclap headache) Fever, rash, and/or stiff neck (meningismus) associated with the headache Papilledema (optic nerve head swelling) Dizziness, unsteadiness, dysarthria, weakness, or changes in sensation (numbness or tingling) especially if profound, static, and occurring for the first time Migraine auras or other previously experienced neurologic migraine accompaniments lasting longer than 1 hr Presence of confusion, drowsiness, or loss of consciousness Headache is triggered by exertion, coughing, bending, or sexual activity Headache is progressively worsening and/or resistant to treatment Previously experienced headache characteristics or accompaniments have substantially changed Persistent or severe vomiting accompanies the headache Headaches beginning after age of 50 are associated with a higher risk of arteritis or intracranial tumors. Inquire about unexplained weight loss, sweats, fevers, myalgia, arthralgia, and jaw claudication, which are typical accompaniments of giant cell (temporal) arteritis Headache occurring in a patient with human immunodeficiency virus or cancer Frequent emergency department or acute care use Daily or near-daily use of pain relievers or the need to take more than the recommended dosage of pain relievers to control headache symptoms
TABLE 42–3 Indications for Neuroimaging in Headaches
Urgent Thunderclap headache with neurologic deficit Headache with altered mental status or seizure Prior intervention (if reduced intracranial compliance focal defects suspected, meningismus) Routine Thunderclap headache without focal neurologic deficit Change in headache characteristics (severity, side shift, worsening) Headache accompanied by neurologic deficit or abnormality (disequilibrium, pronator drift, weakness, papilledema) Headache in immunocompromised patients, cancer patients
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pain is alleviated within 2 weeks of treatment with antiinflammatory medications. Imaging studies are needed to rule out carotid dissection and in some cases CT aspiration of amorphous calcific material from the swollen periverterbal tissues.6 Acute retropharyngeal tendinitis typically occurs in the third through sixth decade of life and presents as a triad of neck pain, odynophagia, and fever. Treatment is usually conservative and includes NSAIDS or a short course of corticosteroids and it is self-limited in most cases.7,8
CRANIOCERVICAL DYSTONIA
FIGURE 42-1 Paranasal sinus.
RETROPHARYNGEAL TENDONITIS Retropharyngeal tendonitis (also called longus colli tendonitis) is described as either unilateral or bilateral nonpulsatile pain in the posterior neck radiating to the occiput or entire head accompanied by swollen prevertebral soft tissue measuring more than 7 mm in adults anterior to the upper cervical vertebral bodies. The pain is exacerbated by neck extension, and less commonly with neck rotation and swallowing. The transverse process of the upper three vertebral bodies is tender to palpation. The
Craniocervical dystonia (CCD) is characterized by crampy or “tension-type pain” in the posterior neck radiating to the occiput or entire head accompanied by defective posture of the head or neck due to muscular hyperactivity. The pain is exacerbated by muscle contraction, movement, external pressure, or sustained posture. The pain resolves within 3 months of successful treatment of the underlying muscle hyperactivity. These dystonias include pharyngeal dystonia, spasmodic torticollis, mandibular dystonia, or lingual dystonia.9 The prevalence of craniocervical dystonia was estimated to be 1.1 to 6.1 per 100,000 people with an incidence of 1.1 per 100,000 per year.10,11 Studies on the pathophysiology of CCD suggest functional defects in dopamine signaling.12 Treatment involves physical therapy, muscle relaxants, and botulinum toxin injections.
HEADACHE ATTRIBUTED TO RHINOSINUSITIS This is a secondary cause of frontal headache and pain in one or more region of the face, ears, or teeth that is accompanied by clinical, radiographic, endoscopic, or
TABLE 42–4 Secondary Headaches or Facial Pain Attributed to Disorder of Facial and Cranial Structures
ICHD-2
ICD-10
Diagnosis
11
[G44.84]
11.1 11.2 11.2.1 11.2.2 11.2.3 11.3 11.3.1 11.3.2 11.3.3 11.3.4 11.4 11.5 11.6 11.7 11.8
[G44.840] [G44.841] [G44.841] [G44.842] [G44.841] [G44.843] [G44.843] [G44.843] [G44.843] [G44.843] [G44.844] [G44.845] [G44.846] [G44.846] [G44.84]
Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures Headache attributed to disorder of cranial bone Headache attributed to disorder of neck Cervicogenic headache Headache attributed to retropharyngeal tendonitis Headache attributed to craniocervical dystonia Headache attributed to disorder of eyes Headache attributed to acute glaucoma Headache attributed to refractive errors Headache attributed to heterophoria or heterotropia (latent or manifest squint) Headache attributed to ocular inflammatory disorder Headache attributed to disorder of ears Headache attributed to rhinosinusitis Headache attributed to disorder of teeth, jaws, or related structures Headache or facial pain attributed to temporomandibular joint (TMJ) disorder Headache attributed to other disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth
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TABLE 42–5 Common Intraoral Causes of Oral Pain
Category
Condition
Infections
Herpetic stomatitis Varicella zoster Candidiasis Acute necrotizing gingivostomatitis Allergic reactions (toothpaste, mouthwashes, topical medications) Erosive lichen planus Benign mucous membrane pemphigoid Aphthous stomatitis and aphthous lesions Erythema multiforme Graft-versus-host disease Factitial, accidental (burns: chemical, solar, thermal) Self-destructive behaviors (rituals, obsessive behaviors) Iatrogenic (chemotherapy, radiation) Squamous cell carcinoma Mucoepidermoid carcinoma Adenocystic carcinoma Intracranial tumors Burning mouth syndrome and glossodynia Neuralgias Postviral neuralgias Post-traumatic neuropathies Dyskinesias and dystonias Vitamin deficiencies (B12, folate) Mineral deficiencies (iron) Diabetic neuropathy Malabsorption syndromes Xerostomia, secondary to intrinsic or extrinsic conditions Referred pain from esophageal or oropharyngeal malignancy Mucositis secondary to esophageal reflux Angioedema
Immune/autoimmune
Traumatic and iatrogenic injuries
Neoplasia FIGURE 42-2 TM joint articular disorders. Neurologic
laboratory evidence of acute rhinosinusitis (Fig. 42-2). Clinical causes include purulence within the nasal cavity, nasal obstruction, new onset hyposmia/anosmia, and/or fever. The headache/facial pain onset must be congruent with the acute rhinosinusitis and must resolve within 7 days after remission or successful treatment. Conditions that are not considered as causing this headache include deviated septum, nasal turbinate hypertrophy, and sinus membrane atrophy. Chronic sinusitis is not validated as a cause of headache or facial pain unless there is an underlying acute exacerbation.
HEADACHE ATTRIBUTED TO DISORDER OF TEETH, JAWS, OR RELATED STRUCTURES Disorders of the teeth, jaws, or related structures typically cause toothache and facial pain, and less commonly headache. Pain from the teeth may be referred and cause diffuse headache, as in periodontitis or pericoronitis as a result of infection or traumatic irritation around the wisdom teeth. The pain is both temporally and structurally related to a disorder of the teeth and/or jaw and is relieved within 3 months of successful treatment of the underlying pathology. Acute periodontal nociceptive pain is treated with rest (reduced mechanical stimulation), NSAIDs, topical local anesthetics, and analgesics. Chronic periodontal disease is an immune mediated inflammatory process that results in destruction of the teeth and the surrounding anchoring bone.13 Typically, intraoral lesions are self-limited and resolve within a few weeks. If symptoms persist, dental or ENT referral is warranted. Some common painful mucosal conditions are listed in the Table 42-5.14
Nutritional and Metabolic
Miscellaneous
Source: Adapted from Mehta NR, Scrivani SJ, Maciewicz R: Dental and facial pain. In Benzon HT, et al, editors: Raj’s practical management of pain, ed 4, Philadelphia, 2008, Mosby/Elsevier, pp 505–528.
HEADACHE OR FACIAL PAIN ATTRIBUTED TO TEMPOROMANDIBULAR JOINT DISORDER This is characterized by recurrent pain in one or more regions of the head/face from the temporomandibular joint (TMJ). It is precipitated by jaw movements, chewing, decreased or irregular range of motion, and TMJ tenderness that resolves within 3 months after successful treatment of TMJ disorder. These disorders include disc displacements, osteoarthritis, or joint hypermobility, rheumatoid arthritis, and can be associated with myofascial pain and headache.
The temporomandibular joint is a bicondylar joint that contributes to the important functions of mastication and speech. The joint is unique in that the articular surface is covered by fibrocartilage instead of hyaline cartilage. A fibrocartilaginous disc is located between the condyle and and the articular fossa and separates the joint cavity into the superior ad inferior compartment.15 Intracapsular disorders include rheumatoid arthritis, osteoarthritis, and articular disc displacement (Fig. 42-3), while extracapsular disorders include myofascial masticatory pain (Fig. 42-4). Bruxism is hypothesized to contribute
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to TMJ pain secondary to myofascial strain, tooth attrition, capsulitis, and adhesion formation. Radiographic examination is usually not helpful. However, when severe symptoms persist after failure of conservative management (splints), periapical radiographs, CT, or MRI is warranted. MRI should not dictate therapy, as asymptomatic individuals have evidence of disc displacement. Treatment includes treatment of any secondary causes such as infection, treatment of somatization component (stress, anxiety), elimination of nocturnal clenching, jaw exercises, and pharmacologic therapy (muscle relaxants, neuropathic pain medications), anti-inflammatory medications). Local anesthetic/steroid and/or botolinum toxin injections may be indicated in selected cases.16–18 Surgery should be considered in patients who do not respond to conservative treatment if anatomic disruption is noted.15 The procedures include total and partial meniscectomy, disk repair, lysis of adhesions, lavage, and in rare instances total joint arthroplasty.15,19 Total TMJ replacement has a poor outcome.
CRANIAL NEURALGIAS AND CENTRAL CAUSES OF FACIAL PAIN AND OTHER HEADACHES These headache and facial pain disorders are the most recognized causes of severe morbidity, none more so than trigeminal neuralgia. Table 42-6 allows for a coherent approach to the cranial neuralgias, and we will focus on the disorders that can elicit oral and facial pain.
TRIGEMINAL NEURALGIA (TIC DOULOUREUX) FIGURE 42-3 TM muscle disorders.
FIGURE 42-4 Trigeminal neuralgia.
Trigeminal neuralgia is a unilateral pain disorder characterized by brief painful episodes described as is typically classified as intense, sharp, and stabbing within the innervation of the one or more divisions of the trigeminal nerve. The disorder usually starts in the second or third divisions (Fig. 42-4), with the first division affected in less than 5% of the patients (Table 42-7). The right side is more frequently affected, in a 3:2 ratio.20 Involvement of the first division hints towards a postinfectious HSV. The duration of the paroxysmal attack can vary from seconds to 2 min and may be precipitated by trivial stimuli from the trigeminal nerve (such as small trigger areas in the nasolabial folds) or by stimuli remote to the trigeminal area, such as other sensory stimulation (i.e., lights, sounds, or tastes). It may occur spontaneously without any identified triggers. If there is a causative lesion identified, outside of vascular compression, then trigeminal neuralgia is secondary, or “symptomatic trigeminal neuralgia.” Concomitantly, there is no clinically evident gross neurologic deficit. The pain is usually unilateral, although bilateral presentations have been reported with more central causes like multiple sclerosis. In between attacks, the patient is normally asymptomatic, although some people with longstanding trigeminal neuralgia report a dull background pain. There also appears to be a refractory period, where another attack cannot be elicited.
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TABLE 42–6 Secondary Headaches Attributed to Cranial Neuralgias and Central Causes of Facial Pain
ICHD-2
ICD-10
Diagnosis
13 13.1 13.1.1 13.1.2 13.2 13.2.1 13.2.2 13.3 13.4 13.5 13.6 13.7 13.8 13.9 13.10
[G44.847, G44.848, or G44.85] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.851] [G44.801]
Cranial neuralgias and central causes of facial pain Trigeminal neuralgia Classical trigeminal neuralgia Symptomatic trigeminal neuralgia Glossopharyngeal neuralgia Classical glossopharyngeal neuralgia Symptomatic glossopharyngeal neuralgia Nervus intermedius neuralgia Superior laryngeal neuralgia Nasociliary neuralgia Supraorbital neuralgia Other terminal branch neuralgias Occipital neuralgia Neck-tongue syndrome External compression headache
13.11 13.11.1 13.11.2 13.12
[G44.802] [G44.8020] [G44.8021] [G44.848]
13.13 13.14 13.15 13.15.1 13.15.2 13.16 13.17 13.18 13.18.1 13.18.2 13.18.3 13.18.4 13.18.5 13.19
[G44.848] [G44.848] [G44.881 or G44.847] [G44.881] [G44.847] [G44.850] [G43.80] [G44.810 or G44.847] [G44.847] [G44.810] [G44.847] [G44.847] [G44.847] [G44.847]
Cold-stimulus headache Headache attributed to external application of a cold stimulus Headache attributed to ingestion or inhalation of a cold stimulus Constant pain caused by compression, irritation, or distortion of cranial nerves or upper cervical roots by structural lesions Optic neuritis Ocular diabetic neuropathy Head or facial pain attributed to herpes zoster Head or facial pain attributed to acute herpes zoster Postherpetic neuralgia Tolosa-Hunt syndrome Ophthalmoplegic “migraine” Central causes of facial pain Anesthesia dolorosa Central poststroke pain Facial pain attributed to multiple sclerosis Persistent idiopathic facial pain Burning mouth syndrome Other cranial neuralgia or other centrally mediated facial pain
TABLE 42–7 Distribution of Pain in Idiopathic Trigeminal
Neuralgia Trigeminal Division V1 only V2 only V3 only V1 and V2 V2 and V3 V1, V2, and V3
Prevalence 4% 17% 15% 14% 32% 17%
Source: Adapted with changes from Rozen TD: Trigeminal neuralgia and glossopharyngeal neuralgia. Neurol Clin 22:185–206, 2004.
The incidence of trigeminal neuralgia is 4 to 13/100,000 people,20 with approximately 15,000 new cases annually in the United States.21 Females are 1.5 times more likely to have trigeminal neuralgia then men. The pathogenesis of trigeminal neuralgia appears to be most commonly caused by compression of the trigeminal root by tortuous or aberrant vessels, as identified by MRI. The trigeminal nerve is the fifth cranial nerve and resides in the Meckel’s cavity posterolateral to the cavernous sinus adjacent to the sphenoid bone. Medial to the ganglion in Meckel’s cavity is the internal carotid artery, which is located in the posterior portion of the cavernous sinus. The ophthalmic division (V1) courses in the lateral wall of the cavernous sinus and exits via the superior orbital fissure. The maxillary division (V2) exits the skull
CHAPTER 42 Orofacial Pain
base through the foramen rotundum inferolateral to the cavernous sinus. It then enters the pteyrogopalatine fossa. The manibular (V3) component courses along the base of the skull and exits the cranium via the foramen ovale. Treatment centers on prevention and abortive therapy. There have been few systematic reviews describing treatment approaches.22–24 Trigeminal neuralgia usually responds to pharmacotherapy and should be employed before interventions are attempted. Generally, after patients fail conservative treatment, young patients with MRI evidence of vascular compression should be considered for microvascular decompression. Elderly patients or those with no evidence of vascular compression may be a candidate for gamma knife or radiofrequency thermoablation. Conservative treatment strategies include antidepressants and antiepileptics. First-line therapy is carbamazepine or oxycarbamazepine, while second-line treatment is baclofen. Other neuropathic pain medications have been trialed in treatment, but there has been no clear evidence for efficacy.22 Interventional modes of treatment include decompressive, ablative, and neuromudulatory strategies using surgical and percutaneous routes22,25–32 (Table 42-8).
GLOSSOPHARYNGEAL NEURALGIA Glossopharyngeal neuralgia is an uncommon facial pain syndrome characterized by transient severe, sharp, stabbing pain experienced in the ear, base of tongue, tonsillar fossa, or beneath the angle of the jaw. It is unilateral in presentation, lasts for seconds to 2 min, and may be precipitated by swallowing, talking, coughing, chewing, or yawning. The incidence is between 0.2% and 1.3% of trigeminal neuralgia and typically begins after the sixth decade.20 The pain is transmitted via the auricular and pharyngeal branches of the glossopharyngeal nerve, along with the auricular and pharyngeal branches of the vagus nerve. Approximately 2% of patients lose consciousness
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during the pain paroxysms. If a causative lesion is identified, then the neuralgia is secondary, and becomes “symptomatic glossopharyngeal neuralgia.”33 The glossopharyngeal nerve exits the brain stem and descends through the base of the skull through the jugular foramen. It has contributions from the solitary nucleus, the nucleus ambiguous, and the inferior salivatory nucleus. Its branches include the tympanic, stylopharyngeal, tonsillar, carotid sinus, linguinal branches, and communicating branches to the vagus nerve. Vascular impingement of the nerve roots has been implicated in the pathophysiology of glossopharyegnal neuralgia, commonly microvascular compression by the posterior cerebellar artery. 34 Treatment is primarily conservative medical management with anticonvulsants and analgesics. Refractory cases to conservative management are candidates for surgical or percutaneous treatments, including lesioning and nerve blocks.
NERVUS INTERMEDIUS NEURALGIA (GENICULATE NEURALGIA, RAMSAY-HUNT SYNDROME) This is a rare disorder characterized by transient bouts of pain in the internal auditory canal, not attributed to any structural lesion, and is intermittent in onset and may last for seconds to minutes. Disorders of salivation, lacrimation, or taste can accompany the pain and are commonly associated with herpes zoster. Typical cases of Ramsay-Hunt Syndrome (RHS) demonstrate the triad of auricular vesicles, ipsilateral facial palsy, and vestibular/cochlear symptoms. Nervus intermedius neuralgia typically occurs after the fifth decade.34 The nervus intermedius is part of the facial nerve (cranial nerve VII) and is located between the motor component of the facial nerve and the vestibulocochlear nerve (cranial nerve VIII). It contains sensory branches (external auditory meatus, floor of mouth, and palate, and
TABLE 42–8 Interventional Approaches to Trigeminal Neuralgia
A. Surgical Approaches Microvascular decompression (MVD)
The vessels in contact with the trigeminal root entry zone are coagulated or separated from the nerve using an inert sponge.25
B. Percutaneous Approaches Gamma knife Percutaneous balloon microcompression Percutaneous glycerol rhizolysis Percutaneous radiofrequency thermocoagulation Pulsed radiofrequency ablation (RFA)
Stereotactic radiation therapy: high dose of irradiation to a small section of the trigeminal nerve leading to nonselective damage.26 Pressure-induced ischemia. The technique may be more suitable for treatment of V1 trigeminal neuralgia of the first branch as the corneal reflex tends to remain intact.27,28 Under fluoroscopy, predetermined volume of glycerol is injected for neurolysis.29 This is usually considered for the elderly patient who is high risk for surgical MVD. The outcome may be less favorable than MVD, but it is less invasive with lower morbidity and mortality rates.22 Although it would seem a safer alternative than the commonly used thermal RFA, its efficacy is questioned in a randomized controlled study.30
C. Neuromodulation Gasserian ganglion
Neuromodulation stimulation was reported either via a subtemporal craniotomy,31 or a percutaneous approach.32
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mucosa of nose, and provides taste to the anterior two thirds of tongue,) and parasympathetic fibers (superior salivatory nucleus) of the facial nerve. It joins the motor root of the facial nerve in the facial canal, at the geniculate ganglion. Conservative treatment involves the use of neuropathic pain medications. The treatment of herpes zoster, if RHS is suspected, or surgical decompression.35
SUPERIOR LARYNGEAL NEURALGIA This is characterized by severe pain paroxysms, lasting seconds to minutes, in the lateral aspect of the throat and submandibular region and underneath the ear, precipitated by swallowing, shouting, or turning of the head. A trigger point is identified along the lateral aspect of the ipsilateral hyoid bone or hyothyroid membrane that is relieved by superior laryngeal nerve block, ablation, and/or resection of the superior laryngeal nerve. The superior laryngeal nerve is a terminal branch of the vagus nerve (cranial nerve X) and receives sympathetic input from the superior cervical ganglion. It divides into the internal and external superior laryngeal nerve (which innervates the cricothyroid muscle). The recurrent laryngeal nerve innervates all other laryngeal muscles, particularly the abductors, and when damaged can cause vocal cord paralysis (injury results in unilateral adduction of vocal cord) and bilaterally can cause airway obstruction.
NASOCILIARY NEURALGIA (CHARLIN’S NEURALGIA) This is a transient, lancinating pain in the nostril that radiates to the medial/frontal region. It lasts seconds to hours. It is precipitated by touching the ipsilateral nostril and abolished by blockade of the nasociliary nerve. The nasociliary nerve is a branch of the ophthalmic nerve (V1) and enters the orbit between the lateral rectus muscles and continues obliquely beneath the superior rectus and superior oblique muscle to the medial wall of the orbital cavity. The terminal branches include the posterior ethmoidal nerve, the long cilliary nerves, the infratrochlear nerve, the communicating branch of the ciliary ganglion, and the anterior ethmoidal nerve.
SUPRAORBITAL NEURALGIA This pain disorder is characterized by transient or constant pain in the forehead and supraorbital area supplied by the supraorbital nerve (terminal branch of the ophthalmic nerve V1). The pain can be precipitated or reproduced by pressure over the nerve in the supraorbital notch and diagnosis is confirmed by pain relief with local anesthetic blockade.
OTHER TERMINAL BRANCH NEURALGIAS These causes of facial pain are usually caused by neuritis of the terminal peripheral branches of the trigeminal nerve, exclusive to the nasociliary and supraorbital nerves. Pain is characterized by constant or transient pain in an
area innervated by the trigeminal terminal branches. There is tenderness over the affected nerve, which is abolished by local anesthetic blockade. The terminal branches of the trigeminal nerve include the infraorbital, lingual, alveolar, and mental nerves (Fig. 42-5).
OCCIPITAL NEURALGIA Occipital neuralgia is described as paroxysmal stabbing and sharp pain in the distribution of the greater or lesser occipital nerves or third occipital nerve, sometimes accompanied by paresthesia or dysesthesia or tenderness overlying the nerve that is involved. This is discussed in Chapter 41. The constant pain is caused by compression, irritation or distortion of cranial nerves or upper cervical roots by structural lesions.
OPTIC NEURITIS Optic neuritis is described as pain behind one or both eyes accompanied by central vision impairment due to a central or paracentral scotoma. It is not caused by compressive lesion but is thought to be due to optic nerve (CNII) inflammation. The onset of pain and visual impairment are separated by less than 1 month and the pain is self-limited with resolution within 4 weeks. If pain precedes the visual impairment by more than 4 weeks, then it is classified as “probable optic neuritis.” Optic neuritis is often a presenting manifestation of multiple sclerosis.
OCULAR DIABETIC NEUROPATHY This condition is described as pain around the eye and forehead with paresis of one or more ocular cranial nerves in a patient with diabetes mellitus. Usually the pain is centered on one eye with pain developing over approximately 2 hr. The cranial nerve paresis is most commonly the third cranial nerve (oculomotor) and less commonly, the fourth (trochlear) and sixth (abducens) cranial nerves. The neuropathy typically develops within 7 days of onset of pain and is not attributed to another disorder. It is important to rule out other causes of cranial nerve palsies, including infection, infarction, hemorrhage, or neoplasm. Consequently, appropriate neuroimaging and perhaps biopsy is warranted.
HEAD OR FACIAL PAIN ATTRIBUTED TO HERPES ZOSTER Head or facial pain can be caused by herpes zoster. The pain usually precedes the herpetic eruption by less than 7 days, and the pain is congruent with herpetic nerve eruption. Typically, pain resolves within 3 months. The herpetic zoster affects the trigeminal nerve in approximately 10% of patients, with the V1 or ophthalmic division most commonly affected (80% of the time) (Fig. 42-6). In contrast, idiopathic trigeminal neuralgia usually affects the V2/3 distribution. Herpetic lesions of the face are not confined to the trigeminal system; it can also involve the geniculate ganglion (causing an eruption near the external auditory meatus). Consequently, ophthalmic herpes can be associated with third, fourth, and
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FIGURE 42-5 Dermatomes head and neck lateral.
six cranial nerve palsies. Zoster can be a harbinger for a more insidious disease process, as it occurs in 10% of patients with lymphoma and 25% of patients with Hodgkin’s disease. Postherpetic neuralgia (PHN) is facial pain in the distribution of the affected nerve that persists 3 months after the skin eruptions. Herpes zoster infection increases with age, with an incidence of 3.4/1000 people per year overall, with more than 10/1000 in patients over the age of 65.36 Similarly, it afflicts 50% of patients who have contracted zoster over the age of 60 years and the incidence continues to increase with advanced age.37 The pathophysiology of acute herpes zoster correlates with the replication of varicella zoster virus and spread within the dorsal root or ganglion and along the peripheral sensory nerve. It may disseminate locally to adjacent structures, including the spinal cord. The characteristic dermatomal distribution is related to the anatomical or functional disruption of the nervous system. Necrosis of the dorsal root ganglion, the presence of the virus within the nerve elements, and atrophy of the dorsal horn characterize PHN. The exact underlying mechanism remains unclear despite the identified pathological changes, although deafferentation, adrenergic receptor activation, and reduction in presynaptic inhibition may contribute to central sensitization.38–40 Management of herpetic pain includes antiviral medications. The more bioavailable medications valaciclovir and
famciclovir are more effective than acyclovir41 in treating acute herpes zoster. The efficacy of steroid use is equivocal. Neuropathic pain medications include anticonvulsants (gabapentin, pregabalin) and antidepressants (amitriptyline, nortriptyline). Other medications commonly employed include topical agents (lidocaine patch), capsacin, opioids, and NMDA antagonists. Sympathetic blockade (e.g., stellate ganglion blockade) may be helpful specially if performed within the first year.42 In extreme cases, some patients may resort to surgery, including cordotomy, rhizotomy, sympathetcomy, trigeminal tractomy, mesencepalotomy, retrogasserian rhizotomy, or superfical greater petrosal neurotomy.43
TOLOSA-HUNT SYNDROME This syndrome is characterized by episodic orbital pain with paralysis of one or more of the third, fourth, and sixth cranial nerves that resolves spontaneously. Usually, it has a waxing and waning course. The unilateral orbital pain can persist for weeks if untreated. There may be a granuloma demonstrated radiographically or noted via a biopsy. It is a painful ophthalmoplegia; the pain and paresis occur within 2 weeks of onset and resolve within 72 hr of treatment with corticosteroids. It can also involve divisions of the trigeminal nerve, along with the facial, optic, and acoustic nerves. It is important to carefully exclude other causes of the painful ophthalmoplegia including inflammatory
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(vasculitis, sarcoid), infectious (meningitis), and endocrinologic (diabetes mellitus) causes. It may also be due to cancer (pain is due to a mass effect) or to a primary headache (migraine).
CENTRAL CAUSES OF FACIAL PAIN Central causes of facial pain include anesthesia dolorosa, central poststroke pain, facial pain secondary to multiple sclerosis, persistent idiopathic facial pain, and burning mouth syndrome. The pathophysiology is poorly elucidated; however, two processes have been implicated: neuritis with reduction in nerve threshold for a given painful stimulus or a reduction in inhibition from “loss of inhibition.” Characteristically, the pain complaint can vary significantly. The pain may be cramping, constricting, crushing, or shooting/lancinating in character. There may be a pins and needles sensation or dysethesia. Physical examination may show allodynia. Triggering stimuli include extreme temperatures and emotional distress.
ANESTHESIA DOLOROSA Anesthesia dolorosa is a painful anesthesia or hypesthesia in the distribution of the trigeminal, or one of its divisions, or occipital nerve. It is caused by a lesion of the relevant nerve or its central connections and is characterized as persistent pain with diminished sensory loss in the distribution of the nerve. It is often related to surgical trauma via rhizotomy or thermocoagulation of the occipital nerve or the trigeminal ganglion. Anesthesia dolorosa was reported in up to 1.6% and 3% of cases after glycerol rhizotomy and radiofrequency rhizotomy, respectively, in the treatment of trigeminal neuralgia.22,44,45
CENTRAL POSTSTROKE PAIN Central poststroke pain is a unilateral pain and dysesthesia associated with loss of sensation to pinprick, touch, and temperature of the ipsilateral face. There is usually a history of symptoms suggestive of stroke, with a lesion demonstrated radiographically. The pain and dysesthesia develop within 6 months after the stroke, is usually persistent, and is usually attributed to a lesion of the trigeminothalamic pathway, thalamus, or thalamocortical projection. It may affect the trunk and limbs on the ipsilateral or contralateral side. Some estimate prevalence of 8% to 11% in patients who have had a stroke.46
FACIAL PAIN ATTRIBUTED TO MULTIPLE SCLEROSIS This is characterized by unilateral or bilateral facial pain with or without an associated dysesthesia attributed to a demyelinating lesion in the pons or trigeminothalamic pathway in patients who have multiple sclerosis. In young people with trigeminal neuralgia and side-switch, one needs to be suspicious of multiple sclerosis. Trigeminal neuralgia occurs in 1% to 2% of patients with multiple sclerosis.47
PERSISTENT IDIOPATHIC FACIAL PAIN (ATYPICAL FACE PAIN) This is facial pain that is present daily and persists for the majority of the day, but does not have features attributed to any of the other cranial neuralgias. It is confined to a poorly defined area of the face and is “deep” in location, not associated with sensory loss or other physical signs. It is not attributed to any other disorder. The pain is commonly in the nasolabial fold or side of the chin and may spread to the upper or lower jaw with a more generalized distribution. It may be triggered by surgery or injury to the face, cheek, and gums. Like ophthalmoplegias, atypical face pain can be a harbinger of a disease. Ipsilateral lung carcinoma can be preceded by referred ear, facial, or temple pain secondary to invasion of the vagus nerve. Education, counseling, and support are essential components of the management strategy. Few reports suggest a role for sphenopalatine ganglion block and radiofrequency ablation in intractable cases.48
BURNING MOUTH SYNDROME This pain is characterized by an intraoral burning sensation wherein no medical or dental etiology is demonstrated. The mouth pain is daily and persistent for most of the day. Associated symptoms include subjective dryness of the mouth, paresthesia, and altered taste. This condition predominately affects woman, and 30% to 50% of patients improve spontaneously.
CONCLUSION
FIGURE 42-6 Acute and postherpetic neuralgia.
Oral and facial pain can be an overwhelming complex diagnostic exercise. However, with a careful history, and detailed examination, an appropriate treatment plan can be employed. The etiology and complex interrelationships
CHAPTER 42 Orofacial Pain
affect the clinical presentation, and the need for a multidisciplinary approach, with the appropriate subspecialty referrals, is crucial for successful treatment.
KEY POINTS l
Diagnosis guides management; an algorithmic approach is necessary to treat patients with headache and facial pain. Accurate diagnosis requires knowledge of the ICHD-2 criteria, and stepwise elimination of primary and secondary headaches.
l
l
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Red flags in the history and physical examination require further investigation. Treatment centers on preventive and abortive strategies. The appropriate timing for interventional treatment needs to be measured against the severity of the impact the pain has on the patient.
REFERENCES Access the reference list online at http://www.expertconsult. com
42
Orofacial Pain Jason E. Pope, MD b Samer Narouze, MD, MSc, DABPM, FIPP
The incidence and prevalence of orofacial pain in the general population is very high. Care and emphasis should be placed on correct diagnosis and treatment rather than on symptomatic management. Each disorder will be described according to the classification and diagnostic criteria published in the International Classification of Headache Disorders, second edition (ICHD-2). The pathophysiology of the disorder, the clinical picture, and the management (both medical and interventional if applicable) will be reviewed. The ICHD-2 criteria provide a systematic classification for headache and orofacial pain and are divided into three parts: the primary headaches, the secondary headaches, and cranial neuralgias central and primary facial pain.1 We will focus mainly on Sections 11 and 13 of the ICHD-2 (Table 42-1). However, before considering the diagnoses that are commonly attributed to orofacial pain, it is relevant to provide a brief comment on eliciting the key components of the history and physical examination in the evaluation of headache and orofacial pain. It is important to take a stepwise, systematic approach to the patients pain. This requires a fundamental knowledge of the ICHD-2 criteria. It should be noted that in one series of 97 consecutive patients presenting to a tertiary care neurologic facility, 29% were not classifiable using the ICHD-2 criteria.2 An appropriate physical examination includes a thorough neurologic assessment (including gait, pronator drift, Romberg’s sign, and reflex testing, that is, Hoffman and Babinski signs), heart and carotid auscultation, fundoscopic examination, cervical range of motion (ROM including atlantoaxial and atlantoocciptial joint), a musculoskeletal evaluation with careful detail to myofascial tenderness and trigger points, maneuvers that provoke radicular signs (Spurling’s test), cervical facet examination, and Waddell’s signs of nonorganic pain (tenderness to palpation, stimulation, distraction, regional disturbance in function, and overreaction). Tables 42-2 and 42-3 list findings and characteristics indicating the need for neuroimaging evaluation, respectively.3
ANATOMY AND PATHOPHYSIOLOGY The trigeminal system provides the relay system for pain and touch sensation to the face, as well as motor function to the muscles of mastication. The trigeminal system is a bilateral structure that spans from the midbrain to the medulla and is composed of four nuclei: the mesencephalic nucleus, the main sensory nucleus, a spinal nucleus of V, and the motor nucleus. The caudal portion of the trigeminal system nucleus is referred to as the spinal nucleus of V and is composed of three regions, in cephalad to caudal order, the subnucleus oralis, the subnucleus interplaris, and the subnucleus caudalis. The subnucleus caudalis is very similar in structure and function to the dorsal horn and extends down to the second or third cervical © Copyright 2011 Elsevier Inc., Ltd., BV. All rights reserved.
level. The primary afferent synapses ipsilaterally in the nucleus caudalis and then the second-order neuron crosses to join the contralateral spinothalamic tract. The trigeminal pathway is termed the ventral trigeminothalamic tract and terminates in the ventral posteromedial (VPM) nucleus of the thalamus. Activation of nuclei in close proximity to the trigeminocervical complex may explain the associated aura and symptoms attributed to different headache disorders by either activation of wide dynamic neurons, ephaptic transmission, or by sheer close proximity to the complex (solitary nucleus, nucleus ambiguous, or dorsal nucleus of vagus nerve). Goadsby demonstrated the trigeminocervical convergence mechanism (Fig. 42-1). He electrically stimulated the superior sagittal sinus of adult monkeys and C-fos was expressed in the superficial laminae of the dorsal horn of C1 and C2, but none in C3.4 Anthony examined patients with occipital headache and he summarized that “projection of pain . . . overlap between trigeminal nucleus and upper cervical cord . . . form a column of cells forming the posterior horn . . . to C4.”5 Consequently, the trigeminocervical complex with the hypothesized reciprocal interactions described by Goadsby, appear to introduce potential neuromudulatory/ablative sites for a variety of headache disorders, contrary to the accepted headache generator foci.
HEADACHE ATTRIBUTED TO DISORDER OF CRANIAL BONE The diagnostic criteria include pain in one or more regions in the head and face with clinical, laboratory, or imaging evidence of a lesion within the cranial bone known to be valid evidence of generating headache (Table 42-4). The source of the pain must be in close temporal association to and is maximal over the bone lesion, and with resolution of the pain after successful treatment of the bone lesion. Most disorders of the skull are not painful, with the exception of osteomyelitis, multiple myeloma, and Paget’s disease.
HEADACHE ATTRIBUTED TO DISORDER OF NECK These constellations of disorders involve pain referral from neck structures to the head/and or face. The diagnostic criteria hinges on what is excepted as “being generally accepted as valid cause of headache.”
CERVICOGENIC HEADACHE Cervicogenic headache is pain attributed to a disorder or lesion within the cervical spine or soft tissues that is generally accepted to cause headache or facial pain. (Please refer to Chapter 41). 283
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TABLE 42–1 ICHD-2 Classification Headings
Part I: The Primary Headaches 1. Migraine 2. Tension-type headache 3. Cluster headache and other trigeminal autonomic cephalalgias 4. Other primary headaches Part II: The Secondary Headaches 5. Headache attributed to head and/or neck trauma 6. Headache attributed to cranial or cervical vascular disorder 7. Headache attributed to nonvascular intracranial disorder 8. Headache attributed to a substance or its withdrawal 9. Headache attributed to infection 10. Headache attributed to disorder of homoeostasis 11. Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cranial structures 12. Headache attributed to psychiatric disorder Part III: Cranial Neuralgias Central and Primary Facial Pain and Other Headaches 13. Cranial neuralgias and central causes of facial pain 14. Other headache, cranial neuralgia, central or primary facial pain
TABLE 42–2 Headache with “Red Flag” Symptoms and Signs That Require Further Work-up
Sudden onset of headache (thunderclap headache) Fever, rash, and/or stiff neck (meningismus) associated with the headache Papilledema (optic nerve head swelling) Dizziness, unsteadiness, dysarthria, weakness, or changes in sensation (numbness or tingling) especially if profound, static, and occurring for the first time Migraine auras or other previously experienced neurologic migraine accompaniments lasting longer than 1 hr Presence of confusion, drowsiness, or loss of consciousness Headache is triggered by exertion, coughing, bending, or sexual activity Headache is progressively worsening and/or resistant to treatment Previously experienced headache characteristics or accompaniments have substantially changed Persistent or severe vomiting accompanies the headache Headaches beginning after age of 50 are associated with a higher risk of arteritis or intracranial tumors. Inquire about unexplained weight loss, sweats, fevers, myalgia, arthralgia, and jaw claudication, which are typical accompaniments of giant cell (temporal) arteritis Headache occurring in a patient with human immunodeficiency virus or cancer Frequent emergency department or acute care use Daily or near-daily use of pain relievers or the need to take more than the recommended dosage of pain relievers to control headache symptoms
TABLE 42–3 Indications for Neuroimaging in Headaches
Urgent Thunderclap headache with neurologic deficit Headache with altered mental status or seizure Prior intervention (if reduced intracranial compliance focal defects suspected, meningismus) Routine Thunderclap headache without focal neurologic deficit Change in headache characteristics (severity, side shift, worsening) Headache accompanied by neurologic deficit or abnormality (disequilibrium, pronator drift, weakness, papilledema) Headache in immunocompromised patients, cancer patients
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285
pain is alleviated within 2 weeks of treatment with antiinflammatory medications. Imaging studies are needed to rule out carotid dissection and in some cases CT aspiration of amorphous calcific material from the swollen periverterbal tissues.6 Acute retropharyngeal tendinitis typically occurs in the third through sixth decade of life and presents as a triad of neck pain, odynophagia, and fever. Treatment is usually conservative and includes NSAIDS or a short course of corticosteroids and it is self-limited in most cases.7,8
CRANIOCERVICAL DYSTONIA
FIGURE 42-1 Paranasal sinus.
RETROPHARYNGEAL TENDONITIS Retropharyngeal tendonitis (also called longus colli tendonitis) is described as either unilateral or bilateral nonpulsatile pain in the posterior neck radiating to the occiput or entire head accompanied by swollen prevertebral soft tissue measuring more than 7 mm in adults anterior to the upper cervical vertebral bodies. The pain is exacerbated by neck extension, and less commonly with neck rotation and swallowing. The transverse process of the upper three vertebral bodies is tender to palpation. The
Craniocervical dystonia (CCD) is characterized by crampy or “tension-type pain” in the posterior neck radiating to the occiput or entire head accompanied by defective posture of the head or neck due to muscular hyperactivity. The pain is exacerbated by muscle contraction, movement, external pressure, or sustained posture. The pain resolves within 3 months of successful treatment of the underlying muscle hyperactivity. These dystonias include pharyngeal dystonia, spasmodic torticollis, mandibular dystonia, or lingual dystonia.9 The prevalence of craniocervical dystonia was estimated to be 1.1 to 6.1 per 100,000 people with an incidence of 1.1 per 100,000 per year.10,11 Studies on the pathophysiology of CCD suggest functional defects in dopamine signaling.12 Treatment involves physical therapy, muscle relaxants, and botulinum toxin injections.
HEADACHE ATTRIBUTED TO RHINOSINUSITIS This is a secondary cause of frontal headache and pain in one or more region of the face, ears, or teeth that is accompanied by clinical, radiographic, endoscopic, or
TABLE 42–4 Secondary Headaches or Facial Pain Attributed to Disorder of Facial and Cranial Structures
ICHD-2
ICD-10
Diagnosis
11
[G44.84]
11.1 11.2 11.2.1 11.2.2 11.2.3 11.3 11.3.1 11.3.2 11.3.3 11.3.4 11.4 11.5 11.6 11.7 11.8
[G44.840] [G44.841] [G44.841] [G44.842] [G44.841] [G44.843] [G44.843] [G44.843] [G44.843] [G44.843] [G44.844] [G44.845] [G44.846] [G44.846] [G44.84]
Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures Headache attributed to disorder of cranial bone Headache attributed to disorder of neck Cervicogenic headache Headache attributed to retropharyngeal tendonitis Headache attributed to craniocervical dystonia Headache attributed to disorder of eyes Headache attributed to acute glaucoma Headache attributed to refractive errors Headache attributed to heterophoria or heterotropia (latent or manifest squint) Headache attributed to ocular inflammatory disorder Headache attributed to disorder of ears Headache attributed to rhinosinusitis Headache attributed to disorder of teeth, jaws, or related structures Headache or facial pain attributed to temporomandibular joint (TMJ) disorder Headache attributed to other disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth
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TABLE 42–5 Common Intraoral Causes of Oral Pain
Category
Condition
Infections
Herpetic stomatitis Varicella zoster Candidiasis Acute necrotizing gingivostomatitis Allergic reactions (toothpaste, mouthwashes, topical medications) Erosive lichen planus Benign mucous membrane pemphigoid Aphthous stomatitis and aphthous lesions Erythema multiforme Graft-versus-host disease Factitial, accidental (burns: chemical, solar, thermal) Self-destructive behaviors (rituals, obsessive behaviors) Iatrogenic (chemotherapy, radiation) Squamous cell carcinoma Mucoepidermoid carcinoma Adenocystic carcinoma Intracranial tumors Burning mouth syndrome and glossodynia Neuralgias Postviral neuralgias Post-traumatic neuropathies Dyskinesias and dystonias Vitamin deficiencies (B12, folate) Mineral deficiencies (iron) Diabetic neuropathy Malabsorption syndromes Xerostomia, secondary to intrinsic or extrinsic conditions Referred pain from esophageal or oropharyngeal malignancy Mucositis secondary to esophageal reflux Angioedema
Immune/autoimmune
Traumatic and iatrogenic injuries
Neoplasia FIGURE 42-2 TM joint articular disorders. Neurologic
laboratory evidence of acute rhinosinusitis (Fig. 42-2). Clinical causes include purulence within the nasal cavity, nasal obstruction, new onset hyposmia/anosmia, and/or fever. The headache/facial pain onset must be congruent with the acute rhinosinusitis and must resolve within 7 days after remission or successful treatment. Conditions that are not considered as causing this headache include deviated septum, nasal turbinate hypertrophy, and sinus membrane atrophy. Chronic sinusitis is not validated as a cause of headache or facial pain unless there is an underlying acute exacerbation.
HEADACHE ATTRIBUTED TO DISORDER OF TEETH, JAWS, OR RELATED STRUCTURES Disorders of the teeth, jaws, or related structures typically cause toothache and facial pain, and less commonly headache. Pain from the teeth may be referred and cause diffuse headache, as in periodontitis or pericoronitis as a result of infection or traumatic irritation around the wisdom teeth. The pain is both temporally and structurally related to a disorder of the teeth and/or jaw and is relieved within 3 months of successful treatment of the underlying pathology. Acute periodontal nociceptive pain is treated with rest (reduced mechanical stimulation), NSAIDs, topical local anesthetics, and analgesics. Chronic periodontal disease is an immune mediated inflammatory process that results in destruction of the teeth and the surrounding anchoring bone.13 Typically, intraoral lesions are self-limited and resolve within a few weeks. If symptoms persist, dental or ENT referral is warranted. Some common painful mucosal conditions are listed in the Table 42-5.14
Nutritional and Metabolic
Miscellaneous
Source: Adapted from Mehta NR, Scrivani SJ, Maciewicz R: Dental and facial pain. In Benzon HT, et al, editors: Raj’s practical management of pain, ed 4, Philadelphia, 2008, Mosby/Elsevier, pp 505–528.
HEADACHE OR FACIAL PAIN ATTRIBUTED TO TEMPOROMANDIBULAR JOINT DISORDER This is characterized by recurrent pain in one or more regions of the head/face from the temporomandibular joint (TMJ). It is precipitated by jaw movements, chewing, decreased or irregular range of motion, and TMJ tenderness that resolves within 3 months after successful treatment of TMJ disorder. These disorders include disc displacements, osteoarthritis, or joint hypermobility, rheumatoid arthritis, and can be associated with myofascial pain and headache.
The temporomandibular joint is a bicondylar joint that contributes to the important functions of mastication and speech. The joint is unique in that the articular surface is covered by fibrocartilage instead of hyaline cartilage. A fibrocartilaginous disc is located between the condyle and and the articular fossa and separates the joint cavity into the superior ad inferior compartment.15 Intracapsular disorders include rheumatoid arthritis, osteoarthritis, and articular disc displacement (Fig. 42-3), while extracapsular disorders include myofascial masticatory pain (Fig. 42-4). Bruxism is hypothesized to contribute
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287
to TMJ pain secondary to myofascial strain, tooth attrition, capsulitis, and adhesion formation. Radiographic examination is usually not helpful. However, when severe symptoms persist after failure of conservative management (splints), periapical radiographs, CT, or MRI is warranted. MRI should not dictate therapy, as asymptomatic individuals have evidence of disc displacement. Treatment includes treatment of any secondary causes such as infection, treatment of somatization component (stress, anxiety), elimination of nocturnal clenching, jaw exercises, and pharmacologic therapy (muscle relaxants, neuropathic pain medications), anti-inflammatory medications). Local anesthetic/steroid and/or botolinum toxin injections may be indicated in selected cases.16–18 Surgery should be considered in patients who do not respond to conservative treatment if anatomic disruption is noted.15 The procedures include total and partial meniscectomy, disk repair, lysis of adhesions, lavage, and in rare instances total joint arthroplasty.15,19 Total TMJ replacement has a poor outcome.
CRANIAL NEURALGIAS AND CENTRAL CAUSES OF FACIAL PAIN AND OTHER HEADACHES These headache and facial pain disorders are the most recognized causes of severe morbidity, none more so than trigeminal neuralgia. Table 42-6 allows for a coherent approach to the cranial neuralgias, and we will focus on the disorders that can elicit oral and facial pain.
TRIGEMINAL NEURALGIA (TIC DOULOUREUX) FIGURE 42-3 TM muscle disorders.
FIGURE 42-4 Trigeminal neuralgia.
Trigeminal neuralgia is a unilateral pain disorder characterized by brief painful episodes described as is typically classified as intense, sharp, and stabbing within the innervation of the one or more divisions of the trigeminal nerve. The disorder usually starts in the second or third divisions (Fig. 42-4), with the first division affected in less than 5% of the patients (Table 42-7). The right side is more frequently affected, in a 3:2 ratio.20 Involvement of the first division hints towards a postinfectious HSV. The duration of the paroxysmal attack can vary from seconds to 2 min and may be precipitated by trivial stimuli from the trigeminal nerve (such as small trigger areas in the nasolabial folds) or by stimuli remote to the trigeminal area, such as other sensory stimulation (i.e., lights, sounds, or tastes). It may occur spontaneously without any identified triggers. If there is a causative lesion identified, outside of vascular compression, then trigeminal neuralgia is secondary, or “symptomatic trigeminal neuralgia.” Concomitantly, there is no clinically evident gross neurologic deficit. The pain is usually unilateral, although bilateral presentations have been reported with more central causes like multiple sclerosis. In between attacks, the patient is normally asymptomatic, although some people with longstanding trigeminal neuralgia report a dull background pain. There also appears to be a refractory period, where another attack cannot be elicited.
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TABLE 42–6 Secondary Headaches Attributed to Cranial Neuralgias and Central Causes of Facial Pain
ICHD-2
ICD-10
Diagnosis
13 13.1 13.1.1 13.1.2 13.2 13.2.1 13.2.2 13.3 13.4 13.5 13.6 13.7 13.8 13.9 13.10
[G44.847, G44.848, or G44.85] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.847] [G44.851] [G44.801]
Cranial neuralgias and central causes of facial pain Trigeminal neuralgia Classical trigeminal neuralgia Symptomatic trigeminal neuralgia Glossopharyngeal neuralgia Classical glossopharyngeal neuralgia Symptomatic glossopharyngeal neuralgia Nervus intermedius neuralgia Superior laryngeal neuralgia Nasociliary neuralgia Supraorbital neuralgia Other terminal branch neuralgias Occipital neuralgia Neck-tongue syndrome External compression headache
13.11 13.11.1 13.11.2 13.12
[G44.802] [G44.8020] [G44.8021] [G44.848]
13.13 13.14 13.15 13.15.1 13.15.2 13.16 13.17 13.18 13.18.1 13.18.2 13.18.3 13.18.4 13.18.5 13.19
[G44.848] [G44.848] [G44.881 or G44.847] [G44.881] [G44.847] [G44.850] [G43.80] [G44.810 or G44.847] [G44.847] [G44.810] [G44.847] [G44.847] [G44.847] [G44.847]
Cold-stimulus headache Headache attributed to external application of a cold stimulus Headache attributed to ingestion or inhalation of a cold stimulus Constant pain caused by compression, irritation, or distortion of cranial nerves or upper cervical roots by structural lesions Optic neuritis Ocular diabetic neuropathy Head or facial pain attributed to herpes zoster Head or facial pain attributed to acute herpes zoster Postherpetic neuralgia Tolosa-Hunt syndrome Ophthalmoplegic “migraine” Central causes of facial pain Anesthesia dolorosa Central poststroke pain Facial pain attributed to multiple sclerosis Persistent idiopathic facial pain Burning mouth syndrome Other cranial neuralgia or other centrally mediated facial pain
TABLE 42–7 Distribution of Pain in Idiopathic Trigeminal
Neuralgia Trigeminal Division V1 only V2 only V3 only V1 and V2 V2 and V3 V1, V2, and V3
Prevalence 4% 17% 15% 14% 32% 17%
Source: Adapted with changes from Rozen TD: Trigeminal neuralgia and glossopharyngeal neuralgia. Neurol Clin 22:185–206, 2004.
The incidence of trigeminal neuralgia is 4 to 13/100,000 people,20 with approximately 15,000 new cases annually in the United States.21 Females are 1.5 times more likely to have trigeminal neuralgia then men. The pathogenesis of trigeminal neuralgia appears to be most commonly caused by compression of the trigeminal root by tortuous or aberrant vessels, as identified by MRI. The trigeminal nerve is the fifth cranial nerve and resides in the Meckel’s cavity posterolateral to the cavernous sinus adjacent to the sphenoid bone. Medial to the ganglion in Meckel’s cavity is the internal carotid artery, which is located in the posterior portion of the cavernous sinus. The ophthalmic division (V1) courses in the lateral wall of the cavernous sinus and exits via the superior orbital fissure. The maxillary division (V2) exits the skull
CHAPTER 42 Orofacial Pain
base through the foramen rotundum inferolateral to the cavernous sinus. It then enters the pteyrogopalatine fossa. The manibular (V3) component courses along the base of the skull and exits the cranium via the foramen ovale. Treatment centers on prevention and abortive therapy. There have been few systematic reviews describing treatment approaches.22–24 Trigeminal neuralgia usually responds to pharmacotherapy and should be employed before interventions are attempted. Generally, after patients fail conservative treatment, young patients with MRI evidence of vascular compression should be considered for microvascular decompression. Elderly patients or those with no evidence of vascular compression may be a candidate for gamma knife or radiofrequency thermoablation. Conservative treatment strategies include antidepressants and antiepileptics. First-line therapy is carbamazepine or oxycarbamazepine, while second-line treatment is baclofen. Other neuropathic pain medications have been trialed in treatment, but there has been no clear evidence for efficacy.22 Interventional modes of treatment include decompressive, ablative, and neuromudulatory strategies using surgical and percutaneous routes22,25–32 (Table 42-8).
GLOSSOPHARYNGEAL NEURALGIA Glossopharyngeal neuralgia is an uncommon facial pain syndrome characterized by transient severe, sharp, stabbing pain experienced in the ear, base of tongue, tonsillar fossa, or beneath the angle of the jaw. It is unilateral in presentation, lasts for seconds to 2 min, and may be precipitated by swallowing, talking, coughing, chewing, or yawning. The incidence is between 0.2% and 1.3% of trigeminal neuralgia and typically begins after the sixth decade.20 The pain is transmitted via the auricular and pharyngeal branches of the glossopharyngeal nerve, along with the auricular and pharyngeal branches of the vagus nerve. Approximately 2% of patients lose consciousness
289
during the pain paroxysms. If a causative lesion is identified, then the neuralgia is secondary, and becomes “symptomatic glossopharyngeal neuralgia.”33 The glossopharyngeal nerve exits the brain stem and descends through the base of the skull through the jugular foramen. It has contributions from the solitary nucleus, the nucleus ambiguous, and the inferior salivatory nucleus. Its branches include the tympanic, stylopharyngeal, tonsillar, carotid sinus, linguinal branches, and communicating branches to the vagus nerve. Vascular impingement of the nerve roots has been implicated in the pathophysiology of glossopharyegnal neuralgia, commonly microvascular compression by the posterior cerebellar artery. 34 Treatment is primarily conservative medical management with anticonvulsants and analgesics. Refractory cases to conservative management are candidates for surgical or percutaneous treatments, including lesioning and nerve blocks.
NERVUS INTERMEDIUS NEURALGIA (GENICULATE NEURALGIA, RAMSAY-HUNT SYNDROME) This is a rare disorder characterized by transient bouts of pain in the internal auditory canal, not attributed to any structural lesion, and is intermittent in onset and may last for seconds to minutes. Disorders of salivation, lacrimation, or taste can accompany the pain and are commonly associated with herpes zoster. Typical cases of Ramsay-Hunt Syndrome (RHS) demonstrate the triad of auricular vesicles, ipsilateral facial palsy, and vestibular/cochlear symptoms. Nervus intermedius neuralgia typically occurs after the fifth decade.34 The nervus intermedius is part of the facial nerve (cranial nerve VII) and is located between the motor component of the facial nerve and the vestibulocochlear nerve (cranial nerve VIII). It contains sensory branches (external auditory meatus, floor of mouth, and palate, and
TABLE 42–8 Interventional Approaches to Trigeminal Neuralgia
A. Surgical Approaches Microvascular decompression (MVD)
The vessels in contact with the trigeminal root entry zone are coagulated or separated from the nerve using an inert sponge.25
B. Percutaneous Approaches Gamma knife Percutaneous balloon microcompression Percutaneous glycerol rhizolysis Percutaneous radiofrequency thermocoagulation Pulsed radiofrequency ablation (RFA)
Stereotactic radiation therapy: high dose of irradiation to a small section of the trigeminal nerve leading to nonselective damage.26 Pressure-induced ischemia. The technique may be more suitable for treatment of V1 trigeminal neuralgia of the first branch as the corneal reflex tends to remain intact.27,28 Under fluoroscopy, predetermined volume of glycerol is injected for neurolysis.29 This is usually considered for the elderly patient who is high risk for surgical MVD. The outcome may be less favorable than MVD, but it is less invasive with lower morbidity and mortality rates.22 Although it would seem a safer alternative than the commonly used thermal RFA, its efficacy is questioned in a randomized controlled study.30
C. Neuromodulation Gasserian ganglion
Neuromodulation stimulation was reported either via a subtemporal craniotomy,31 or a percutaneous approach.32
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mucosa of nose, and provides taste to the anterior two thirds of tongue,) and parasympathetic fibers (superior salivatory nucleus) of the facial nerve. It joins the motor root of the facial nerve in the facial canal, at the geniculate ganglion. Conservative treatment involves the use of neuropathic pain medications. The treatment of herpes zoster, if RHS is suspected, or surgical decompression.35
SUPERIOR LARYNGEAL NEURALGIA This is characterized by severe pain paroxysms, lasting seconds to minutes, in the lateral aspect of the throat and submandibular region and underneath the ear, precipitated by swallowing, shouting, or turning of the head. A trigger point is identified along the lateral aspect of the ipsilateral hyoid bone or hyothyroid membrane that is relieved by superior laryngeal nerve block, ablation, and/or resection of the superior laryngeal nerve. The superior laryngeal nerve is a terminal branch of the vagus nerve (cranial nerve X) and receives sympathetic input from the superior cervical ganglion. It divides into the internal and external superior laryngeal nerve (which innervates the cricothyroid muscle). The recurrent laryngeal nerve innervates all other laryngeal muscles, particularly the abductors, and when damaged can cause vocal cord paralysis (injury results in unilateral adduction of vocal cord) and bilaterally can cause airway obstruction.
NASOCILIARY NEURALGIA (CHARLIN’S NEURALGIA) This is a transient, lancinating pain in the nostril that radiates to the medial/frontal region. It lasts seconds to hours. It is precipitated by touching the ipsilateral nostril and abolished by blockade of the nasociliary nerve. The nasociliary nerve is a branch of the ophthalmic nerve (V1) and enters the orbit between the lateral rectus muscles and continues obliquely beneath the superior rectus and superior oblique muscle to the medial wall of the orbital cavity. The terminal branches include the posterior ethmoidal nerve, the long cilliary nerves, the infratrochlear nerve, the communicating branch of the ciliary ganglion, and the anterior ethmoidal nerve.
SUPRAORBITAL NEURALGIA This pain disorder is characterized by transient or constant pain in the forehead and supraorbital area supplied by the supraorbital nerve (terminal branch of the ophthalmic nerve V1). The pain can be precipitated or reproduced by pressure over the nerve in the supraorbital notch and diagnosis is confirmed by pain relief with local anesthetic blockade.
OTHER TERMINAL BRANCH NEURALGIAS These causes of facial pain are usually caused by neuritis of the terminal peripheral branches of the trigeminal nerve, exclusive to the nasociliary and supraorbital nerves. Pain is characterized by constant or transient pain in an
area innervated by the trigeminal terminal branches. There is tenderness over the affected nerve, which is abolished by local anesthetic blockade. The terminal branches of the trigeminal nerve include the infraorbital, lingual, alveolar, and mental nerves (Fig. 42-5).
OCCIPITAL NEURALGIA Occipital neuralgia is described as paroxysmal stabbing and sharp pain in the distribution of the greater or lesser occipital nerves or third occipital nerve, sometimes accompanied by paresthesia or dysesthesia or tenderness overlying the nerve that is involved. This is discussed in Chapter 41. The constant pain is caused by compression, irritation or distortion of cranial nerves or upper cervical roots by structural lesions.
OPTIC NEURITIS Optic neuritis is described as pain behind one or both eyes accompanied by central vision impairment due to a central or paracentral scotoma. It is not caused by compressive lesion but is thought to be due to optic nerve (CNII) inflammation. The onset of pain and visual impairment are separated by less than 1 month and the pain is self-limited with resolution within 4 weeks. If pain precedes the visual impairment by more than 4 weeks, then it is classified as “probable optic neuritis.” Optic neuritis is often a presenting manifestation of multiple sclerosis.
OCULAR DIABETIC NEUROPATHY This condition is described as pain around the eye and forehead with paresis of one or more ocular cranial nerves in a patient with diabetes mellitus. Usually the pain is centered on one eye with pain developing over approximately 2 hr. The cranial nerve paresis is most commonly the third cranial nerve (oculomotor) and less commonly, the fourth (trochlear) and sixth (abducens) cranial nerves. The neuropathy typically develops within 7 days of onset of pain and is not attributed to another disorder. It is important to rule out other causes of cranial nerve palsies, including infection, infarction, hemorrhage, or neoplasm. Consequently, appropriate neuroimaging and perhaps biopsy is warranted.
HEAD OR FACIAL PAIN ATTRIBUTED TO HERPES ZOSTER Head or facial pain can be caused by herpes zoster. The pain usually precedes the herpetic eruption by less than 7 days, and the pain is congruent with herpetic nerve eruption. Typically, pain resolves within 3 months. The herpetic zoster affects the trigeminal nerve in approximately 10% of patients, with the V1 or ophthalmic division most commonly affected (80% of the time) (Fig. 42-6). In contrast, idiopathic trigeminal neuralgia usually affects the V2/3 distribution. Herpetic lesions of the face are not confined to the trigeminal system; it can also involve the geniculate ganglion (causing an eruption near the external auditory meatus). Consequently, ophthalmic herpes can be associated with third, fourth, and
CHAPTER 42 Orofacial Pain
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FIGURE 42-5 Dermatomes head and neck lateral.
six cranial nerve palsies. Zoster can be a harbinger for a more insidious disease process, as it occurs in 10% of patients with lymphoma and 25% of patients with Hodgkin’s disease. Postherpetic neuralgia (PHN) is facial pain in the distribution of the affected nerve that persists 3 months after the skin eruptions. Herpes zoster infection increases with age, with an incidence of 3.4/1000 people per year overall, with more than 10/1000 in patients over the age of 65.36 Similarly, it afflicts 50% of patients who have contracted zoster over the age of 60 years and the incidence continues to increase with advanced age.37 The pathophysiology of acute herpes zoster correlates with the replication of varicella zoster virus and spread within the dorsal root or ganglion and along the peripheral sensory nerve. It may disseminate locally to adjacent structures, including the spinal cord. The characteristic dermatomal distribution is related to the anatomical or functional disruption of the nervous system. Necrosis of the dorsal root ganglion, the presence of the virus within the nerve elements, and atrophy of the dorsal horn characterize PHN. The exact underlying mechanism remains unclear despite the identified pathological changes, although deafferentation, adrenergic receptor activation, and reduction in presynaptic inhibition may contribute to central sensitization.38–40 Management of herpetic pain includes antiviral medications. The more bioavailable medications valaciclovir and
famciclovir are more effective than acyclovir41 in treating acute herpes zoster. The efficacy of steroid use is equivocal. Neuropathic pain medications include anticonvulsants (gabapentin, pregabalin) and antidepressants (amitriptyline, nortriptyline). Other medications commonly employed include topical agents (lidocaine patch), capsacin, opioids, and NMDA antagonists. Sympathetic blockade (e.g., stellate ganglion blockade) may be helpful specially if performed within the first year.42 In extreme cases, some patients may resort to surgery, including cordotomy, rhizotomy, sympathetcomy, trigeminal tractomy, mesencepalotomy, retrogasserian rhizotomy, or superfical greater petrosal neurotomy.43
TOLOSA-HUNT SYNDROME This syndrome is characterized by episodic orbital pain with paralysis of one or more of the third, fourth, and sixth cranial nerves that resolves spontaneously. Usually, it has a waxing and waning course. The unilateral orbital pain can persist for weeks if untreated. There may be a granuloma demonstrated radiographically or noted via a biopsy. It is a painful ophthalmoplegia; the pain and paresis occur within 2 weeks of onset and resolve within 72 hr of treatment with corticosteroids. It can also involve divisions of the trigeminal nerve, along with the facial, optic, and acoustic nerves. It is important to carefully exclude other causes of the painful ophthalmoplegia including inflammatory
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(vasculitis, sarcoid), infectious (meningitis), and endocrinologic (diabetes mellitus) causes. It may also be due to cancer (pain is due to a mass effect) or to a primary headache (migraine).
CENTRAL CAUSES OF FACIAL PAIN Central causes of facial pain include anesthesia dolorosa, central poststroke pain, facial pain secondary to multiple sclerosis, persistent idiopathic facial pain, and burning mouth syndrome. The pathophysiology is poorly elucidated; however, two processes have been implicated: neuritis with reduction in nerve threshold for a given painful stimulus or a reduction in inhibition from “loss of inhibition.” Characteristically, the pain complaint can vary significantly. The pain may be cramping, constricting, crushing, or shooting/lancinating in character. There may be a pins and needles sensation or dysethesia. Physical examination may show allodynia. Triggering stimuli include extreme temperatures and emotional distress.
ANESTHESIA DOLOROSA Anesthesia dolorosa is a painful anesthesia or hypesthesia in the distribution of the trigeminal, or one of its divisions, or occipital nerve. It is caused by a lesion of the relevant nerve or its central connections and is characterized as persistent pain with diminished sensory loss in the distribution of the nerve. It is often related to surgical trauma via rhizotomy or thermocoagulation of the occipital nerve or the trigeminal ganglion. Anesthesia dolorosa was reported in up to 1.6% and 3% of cases after glycerol rhizotomy and radiofrequency rhizotomy, respectively, in the treatment of trigeminal neuralgia.22,44,45
CENTRAL POSTSTROKE PAIN Central poststroke pain is a unilateral pain and dysesthesia associated with loss of sensation to pinprick, touch, and temperature of the ipsilateral face. There is usually a history of symptoms suggestive of stroke, with a lesion demonstrated radiographically. The pain and dysesthesia develop within 6 months after the stroke, is usually persistent, and is usually attributed to a lesion of the trigeminothalamic pathway, thalamus, or thalamocortical projection. It may affect the trunk and limbs on the ipsilateral or contralateral side. Some estimate prevalence of 8% to 11% in patients who have had a stroke.46
FACIAL PAIN ATTRIBUTED TO MULTIPLE SCLEROSIS This is characterized by unilateral or bilateral facial pain with or without an associated dysesthesia attributed to a demyelinating lesion in the pons or trigeminothalamic pathway in patients who have multiple sclerosis. In young people with trigeminal neuralgia and side-switch, one needs to be suspicious of multiple sclerosis. Trigeminal neuralgia occurs in 1% to 2% of patients with multiple sclerosis.47
PERSISTENT IDIOPATHIC FACIAL PAIN (ATYPICAL FACE PAIN) This is facial pain that is present daily and persists for the majority of the day, but does not have features attributed to any of the other cranial neuralgias. It is confined to a poorly defined area of the face and is “deep” in location, not associated with sensory loss or other physical signs. It is not attributed to any other disorder. The pain is commonly in the nasolabial fold or side of the chin and may spread to the upper or lower jaw with a more generalized distribution. It may be triggered by surgery or injury to the face, cheek, and gums. Like ophthalmoplegias, atypical face pain can be a harbinger of a disease. Ipsilateral lung carcinoma can be preceded by referred ear, facial, or temple pain secondary to invasion of the vagus nerve. Education, counseling, and support are essential components of the management strategy. Few reports suggest a role for sphenopalatine ganglion block and radiofrequency ablation in intractable cases.48
BURNING MOUTH SYNDROME This pain is characterized by an intraoral burning sensation wherein no medical or dental etiology is demonstrated. The mouth pain is daily and persistent for most of the day. Associated symptoms include subjective dryness of the mouth, paresthesia, and altered taste. This condition predominately affects woman, and 30% to 50% of patients improve spontaneously.
CONCLUSION
FIGURE 42-6 Acute and postherpetic neuralgia.
Oral and facial pain can be an overwhelming complex diagnostic exercise. However, with a careful history, and detailed examination, an appropriate treatment plan can be employed. The etiology and complex interrelationships
CHAPTER 42 Orofacial Pain
affect the clinical presentation, and the need for a multidisciplinary approach, with the appropriate subspecialty referrals, is crucial for successful treatment.
KEY POINTS l
Diagnosis guides management; an algorithmic approach is necessary to treat patients with headache and facial pain. Accurate diagnosis requires knowledge of the ICHD-2 criteria, and stepwise elimination of primary and secondary headaches.
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Red flags in the history and physical examination require further investigation. Treatment centers on preventive and abortive strategies. The appropriate timing for interventional treatment needs to be measured against the severity of the impact the pain has on the patient.
REFERENCES Access the reference list online at http://www.expertconsult. com