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29 Facial Pain

29 Facial Pain
The Massachusetts General Hospital Handbook of Pain Management

29
Facial Pain

Martin A. Acquadro and Avine M. Lydon

Pain is the most urgent of symptoms.
—Henry K. Beecher, first chairman of anesthesia at MGH (1904–1976)

I. Neuroanatomy and neurophysiology
II. Psychological aspects
III. Temporomandibular joint dysfunction, temporomandibular muscle dysfunction, and myofascial dysfunction

1. Diagnostic features

2. Clinical characteristics

3. Epidemiology

4. Diagnostic evaluation, imaging studies, and laboratory tests

5. Treatment
IV. Dental disease and dysfunction

1. Diagnostic features

2. Epidemiology

3. Diagnostic evaluation, imaging studies, and laboratory tests

4. Treatment
V. Paranasal sinus area pain and headache

1. Diagnostic features

2. Epidemiology

3. Imaging studies and laboratory tests

4. Treatment
VI. Trigeminal neuralgia

1. Diagnostic features

2. Epidemiology

3. Diagnostic evaluation, imaging studies, and laboratory tests

4. Treatment
VII. Burning mouth syndrome

1. Diagnostic features

2. Epidemiology

3. Diagnostic evaluation, imaging studies, and laboratory tests

4. Treatment
VIII. Deafferentation pain

1. Diagnostic features

2. Epidemiology

3. Diagnostic evaluation, imaging studies, and laboratory tests

4. Treatment
IX. Acute and postherpetic neuralgia

1. Diagnostic features

2. Epidemiology

3. Diagnostic evaluation, imaging studies, and laboratory tests

4. Treatment
X. Periocular pain

1. Diagnostic features

2. Epidemiology

3. Diagnostic evaluation, imaging studies, and laboratory tests

4. Treatment
XI. Periauricular pain

1. Diagnostic features

2. Epidemiology

3. Diagnostic evaluation, imaging studies, and laboratory tests

4. Treatment
XII. Head and neck cancer

1. Diagnostic features

2. Epidemiology

3. Diagnostic evaluation, imaging studies, and laboratory tests

4. Treatment
XIII. Conclusion
Selected Readings

Many medical, dental, and other health specialists are involved in the identification of facial pain, often exposing the patient to a variety of referrals and interventions. Although facial pain is commonly the result of a complex process, it is often approached from the bias of one particular specialty, when a multidiscipline or multidimensional approach would provide a more comprehensive treatment. The many specialists involved in the treatment of facial pain, the rich synaptic connections with the limbic and autonomic systems, the social function of the face, and the highly visible and expressive nature of the face, all together make facial pain unique.
I. NEUROANATOMY AND NEUROPHYSIOLOGY
In the head and neck, afferent inputs converge on the trigeminal brainstem sensory nuclear complex within the pons (analogous to, but cephalad to, the dorsal horn of the cervical spinal cord) and on other cranial nerve nuclei. Multiple areas of convergence and interconnections are present between cranial nerves, cervical nerves, and autonomic nerves within the brainstem, comprising the trigeminal sensory nucleus and extending to the level of C5. Lateral thalamic projections assist in location discrimination, while medial thalamic projections mediate emotional and perceptual responses to pain. Ascending pathways project from the trigeminal sensory nucleus to the thalamus, reticular formation, and hypothalamus.
Depending on the specific sensory, autonomic, or neurochemical input, nociception can be suppressed or facilitated by modulating inputs from above and below the level of the trigeminal nucleus, altering the patient’s perception of pain. Clinical features such as referral patterns, autonomic signs, interference with sleep/wake patterns, and the effect of emotional stimulation can be better understood in the context of this rich area of neural interchange. Peripherally, many facial structures are innervated by branches of multiple nerves producing pathways for referred pain. For example, the periauricular area receives sensory innervation from cranial nerves V, VII, IX, and X and from cervical roots C2 and C3, with referral patterns to the neck, eye, and face. Anatomically encapsulated areas such as the middle ear, the eye, dental pulp, and the closed calvaria are susceptible to compression, potentially expressed as facial pain.
II. PSYCHOLOGICAL ASPECTS
The face and the treatment of facial pain are the most visible examples of the biophysical psychosocial model of pain. The face is a window through which we view the world and, in turn, are viewed. Facial pain is therefore a highly visible form of pain, etched on the most expressive area of the body for all to see. This visibility is emphasized by the term for trigeminal neuralgia, tic douloureux. The lack of privacy encountered by sufferers of facial pain compounds the increased rates of anxiety and depression found in many chronic pain states. In addition, facial pain sufferers may be perceived as angry, sad, or socially negative as a result of the effects of pain on their facial expression.
Psychological factors present before the onset of pain (primary) and as a result of the pain (secondary) are important in the patient’s perception of pain. Modification of the psychological factors can modulate the pain experience. Treatment of anxiety, depression, and sleep disruption should always be undertaken in conjunction with treatment of the primary pain source.
III. TEMPOROMANDIBULAR JOINT DYSFUNCTION, TEMPOROMANDIBULAR MUSCLE DYSFUNCTION, AND MYOFASCIAL DYSFUNCTION
1. Diagnostic features
It is useful to distinguish between true temporomandibular joint (TMJ) abnormalities, temporomandibular muscle dysfunction (TMD: dysfunction and pain of the muscles of mastication), and myofascial dysfunction originating in muscles other than those involved directly with mastication. Myofascial dysfunction with pain is a primary muscle disorder featuring pain and inflammation. When it involves the face, the source of pain may be the head and facial muscles, or muscles of mastication.
Because of their neuroanatomy, muscles of the shoulders and neck can have referral patterns to the face, sinuses, or head. Just as there are involuntary mechanical and muscle compensations in the lower back, hips, and knees associated with lower back and extremity musculoskeletal pathology, so there are instigating, contributing, and perpetuating factors of myofascial pain of the head, neck, and orofacial areas from outside these areas.
2. Clinical characteristics
Temporomandibular joint dysfunction
True pathologic derangement of the TMJ as the principle cause for pain is not common. TMJ damage can be the result of direct trauma, wear and tear from chronic pathologic occlusal forces, extreme limits of TMJ motion, acute dislocation, cancer or some other tissue-destructive process, surgical intervention, or arthritis. Just as magnetic resonance imaging (MRI) abnormalities of the lumbar spine can be found in patients who are asymptomatic, so demonstrable TMJ pathology can be found in asymptomatic individuals. Many subjects have an “abnormal” TMJ that “clicks” or has a deviation or displacement during opening and closing of the mandible, but few have accompanying pain. True TMJ dysfunction with pain deserves assessment by an oral surgeon.
Temporomandibular muscle dysfunction
It is useful to separate TMD from other myofascial pain, as treatment focuses additionally on jaw and occlusal activities. TMD is defined by tenderness in one or more masticatory muscle. Additional clinical features include a reduced mandibular range (<35 mm) between incisors and a clicking or popping of the joint. The pain is commonly described as a dull ache exacerbated by chewing, fluctuating in intensity daily, and associated with remissions lasting months.
A range of terms exists, with a variety of classifications. These include myofascial dysfunction, masticatory myositis, masticatory myalgia, tendomyositis, and fibromyalgia. TMD is characterized by dull aching pain exacerbated by mandibular use, muscle tenderness in at least two masticatory muscle groups, and often a decreased mandibular range of motion. The absence of clinical features referable to the TMJ and the presence of muscle tenderness distinguish this from primary TMJ disorders, although secondary TMJ changes can occur. Tendomyositis involves inflammation and pain at the tendon insertion points at the zygomatic and coronoid arch area following spasm of the temporalis and masseter muscles, often precipitated by prolonged mouth opening during dental treatments.
Myofascial dysfunction
Dysfunction of the muscles of the shoulders, neck, head, and face is relatively common in the general population, and it can aggravate headaches, sinus area pain, and orofacial pain. Fibromyalgia, a type of myofascial dysfunction distinguished as a systemic disease, is characterized by muscle pain and tenderness exacerbated by stress, anxiety, and weather changes; it is accompanied by a variety of generalized symptoms such as fatigue, morning stiffness, irritable bowel syndrome, and migraine. The patient with fibromyalgia may initially present with facial pain and tenderness in the muscles of mastication; it is important to question patients for systemic features and not simply focus on the local complaint. Trauma is a possible trigger of myofascial dysfunction, and a history of trauma should be sought. Direct trauma and whiplash injuries to muscles cause tears, bleeding, and edema, and muscle recruitment results in extension of pain into the neck and shoulders.
3. Epidemiology
Myofascial pain syndromes occur predominantly in women. Masticatory myalgia and myositis occur in younger women (late teens to 40 years), whereas the peak age of presentation of fibromyalgia is older (45 to 55 years). The prevalence of TMD ranges from 6% to 12% of the North American population. Patients complaining of TMD pain are likely to be female (9:1), with an average age of 40 (±16) years. Pain produced by direct trauma to facial muscles is notable for its greater frequency in men (3:1).
4. Diagnostic evaluation, imaging studies, and laboratory tests
There are no imaging techniques or laboratory markers that are useful in the diagnosis or management of myofascial pain syndromes. Radiographs frequently show abnormalities of the TMJ disc position in asymptomatic joints and thus are unhelpful. No specific laboratory tests indicate TMJ or TMD pain. An erythrocyte sedimentation rate (ESR) should be obtained if there is suspicion of temporal arteritis, and concerns about other rheumatologic or immunologic diagnoses dictate additional studies and referral to the appropriate specialist.
Diagnostic evaluation includes a careful and thorough history and physical, focusing on global musculoskeletal pain, myofascial pain of the shoulders, neck, and head, and myofascial pain of TMD and TMJ. Evaluation should include a review of a history of headaches, surgeries, trauma, and psychosocial events and stressors. A review of vocational and avocational activities along with posture, repetitive movements, habits, and sleep patterns should be included. A history of bruxism (clenching and grinding of teeth), awakening in the morning with sore jaw muscles, clicking or grating noises when opening the mouth, and recent or extensive dental work should be elicited. Eating habits, medications, exercise routines, and activities that help or worsen myofascial discomfort should be ascertained.
The physical exam should focus on range of motion of the shoulders, arms, neck, and mandible. An exam of the oral cavity for any lesions that may cause a reflex avoidance pattern, pain on extreme opening of the mandible, and abnormal bite should be checked. Teeth sensitivity, painful muscles, and painful points of insertion should be examined.
5. Treatment
Physical therapy
Treatment modalities include physical therapy consultation and treatment, and an active exercise program, with guidance from a physical therapist.
Pharmacologic therapy
Pharmacologic therapy includes judicious use of nonsteroidal anti-inflammatory drugs (NSAIDs), and very selective use of triclyclic antidepressants (TCAs), analgesics, muscle relaxants, anxiolytics, and, rarely, narcotics. NSAIDs may be used for both their analgesic and their anti-inflammatory properties. There is marked interpatient variability in response to different agents, necessitating trials until the optimal response is obtained. Because of the ceiling effect of NSAIDs, increasing doses beyond the recommended maximum is not useful. NSAIDs are of no proven value in the longterm management of TMJ pain, although large doses may provide short-term relief. Patients who are unable to tolerate NSAIDs may use tramadol hydrochloride, a weak and nonaddicting µ agonist, in a dose of 50 to 100 mg every 6 hours as needed.
Centrally acting muscle relaxants include cyclobenzaprine (Flexeril) and carisoprodol (Soma). These agents decrease excess electromyographic (EMG) activity and muscle spasm. The tertiary amine amitriptyline and the secondary amines desipramine and nortriptyline, in low doses, may improve sleep and act as indirect analgesics by augmenting midbrain serotonin levels. Benzodiazepines such as diazepam decrease muscle spasm, improve sleep, and are anxiolytic. A dose of 5 mg twice daily is useful in initial therapy. Prolonged use of benzodiazepines should be avoided because of their addiction potential.
In patients requiring prolonged treatment of anxiety symptoms, buspirone (BuSpar) 5 mg three times daily is effective with little addiction potential, but it has no muscle relaxant effects. Opioids are useful in decreasing pain in refractory cases but are associated with risks of tolerance, addiction, and dependence.
Trigger point injections and physical therapy
Pressure on active trigger points causes acute pain and produces muscle spasm when the muscle is used, decreasing the range of motion. Trigger points can be localized by pressure and then inactivated by the topical application of vapocoolant spray (dichlorodifluoromethane), allowing stretching exercises to restore muscle mobility. Refractory trigger points can be disrupted physically by dry needling. The injection of local anesthetic (0.5 mL of 0.5% procaine or 1% lidocaine per trigger point), or selected trigger point injections of a mixture of equal volumes of lidocaine 1% and bupivacaine 0.5% can be performed with subsequent physical therapy. This provides more prolonged analgesia, allowing the patient a pain-free period to commence physical therapy, with subsequent use of vapocoolants and stretching exercises at home. Corticosteroids, such as triamcinolone acetonide (Kenalog) in a final concentration of 0.1% can be added to the mixture. Steroid injections should not be repeated any sooner than 6 weeks, as a peau d’orange cosmetic defect may occur.
Psychological therapy
Psychological intervention including biofeedback, relaxation techniques, and cognitive behavioral therapy addressing aversive behaviors when they exist should be considered.
TMH and TMD splint therapy
Advocates of splint therapy suggest that bite occlusion mechanically unloads the TMJ and limits masticatory muscle activity and symptoms of TMD and TMJ. Many anecdotal examples of benefit exist, but clinical studies have not provided evidence to support this traditional practice.
TMJ surgery and dental treatment
Surgery of the joint, including arthroscopy and surgical implants, is associated with high morbidity and a lack of efficacy, unless proper and careful patient selection is utilized by an experienced oromaxillofacial surgeon. Missing teeth and dental malocclusions have an inconsistent relationship to TMJ and TMD pain. Oral appliances such as bite blocks to prevent tooth grinding are not always helpful or predictive in the treatment of TMJ and TMD pain. Dental and occlusal evaluation by an experienced dental specialist is required.
Suggested TMD home treatment regimen
Temporary rest of the TMJ is sometimes helpful. A liquid and soft diet is instituted, and gum chewing is stopped. Wide, uncontrolled opening of the jaw is discouraged. Yawning, coughing, laughing, and the eating of large sandwiches is minimized. A hand or fist placed under the chin helps to hold the jaw in place.
Heat therapy can be useful: a heating pad, warm face cloth, or warm water bottle placed to the sides of the jaw and TMJ area has a soothing and relaxing effect on the muscles. Gentle midline opening and closing exercises of the mandible help to retrain and relax muscles. Use of a vapocoolant spray may also be helpful in reducing movement-induced pain so that exercises designed to improve joint mobility can be tolerated.
Judicious use of NSAIDs may also help. Consider acetaminophen in patients with NSAID sensitivity, or cyclooxygenase-2 (COX-2) inhibitors in patients with a serious risk of bleeding or other relevant history. The use of additional medication should be directed by the physician.
IV. DENTAL DISEASE AND DYSFUNCTION
1. Diagnostic features
Because of the rich innervation of the mouth, pain resulting from tooth or periodontal disease can present with numerous features including local pain, headache, or eye symptoms (photophobia, lacrimation, conjunctival injection). A differential diagnosis should include trigeminal neuralgia, sinusitis and other sinus disease, central nervous system (CNS) pathology, cluster, migraine, and muscle contraction tension-type headaches, and myofascial pain of the shoulders, neck, head, and masticatory muscles with referral.
2. Epidemiology
Dental disease is common in men, women, and children of all ages.
3. Diagnostic evaluation, imaging studies, and laboratory tests
During the history and physical examination, dental pathology must be adequately assessed. If dental disease is obvious, then the appropriate referral should be made. However, if dental disease, oral mucosal disease, and pathologic occlusal forces have been ruled out, other pathology must be considered. Problems such as sinusitis; undiagnosed sinus diseases such as cysts, Wegener’s granulomatosis, mucocele, or latent fungal or bacterial infections; undiagnosed and uncategorized headache; chronic allergies; and CNS pathology can mimic dental pain. Computed tomography (CT) or MRI may be indicated.
4. Treatment
Patients should be referred to a dentist, otolaryngologist, or neurologist for further management to rule out organic and treatable pathology. If treatable conditions have been ruled out, however, and there are no obvious sources except a prior history of disease and pain, peripheral or central neuroplastic changes or deafferentation should be considered. Treatment should be directed toward a comprehensive and neuropathic approach, with due consideration of the biophysical psychosocial model of pain treatment. In addition, a late-declaring dental or other problem may appear and be treatable.
V. PARANASAL SINUS AREA PAIN AND HEADACHE
1. Diagnostic features
Acute sinusitis presents with bilateral or unilateral throbbing or sharp facial pain. In the acute setting, diagnosis is usually straightforward. Frequently, pain is exacerbated by leaning forward. A sense of pressure is described by 74% of patients. Medial orbital pain with radiation to the temple is a feature of ethmoid sinusitis. Frontal sinusitis features forehead pain and headache; maxillary sinusitis is suggested by pain over the maxilla, or it may be referred to the occiput, forehead, or orbit.
Chronic sinus area pain presents more of a diagnostic dilemma. Pain that is perceived as emanating from the sinuses can have other causes, including referred pain from dental, dural, and musculoskeletal areas. The differential diagnosis includes myofascial pain, vascular and other types of headache, neuralgias, allergies, and dental disease. Other diagnostic features of sinusitis include purulent discharge from the nasal passages or nasopharynx, intermittent fever, smell or taste disorder, tenderness on tapping the maxillary teeth, and tenderness over the maxillary, frontal, or ethmoidal sinuses. A history of recurrent injury in the form of upper respiratory tract infections and allergies may be elicited. A combination of history, anterior endoscopic examination, and CT findings is required to accurately diagnose sinusitis, particularly prior to embarking on surgical treatments.
2. Epidemiology
There are no distinctive epidemiologic features.
3. Imaging studies and laboratory tests
Endoscopic examination is useful in demonstrating inflamed turbinates, sinus ostia edema, and purulent nasopharyngeal discharge. CT imaging reveals opacification of the sinuses and occluded ostiomeatal complexes. Additional abnormalities may be demonstrated on imaging, including chronic maxillary atelectasis, mucocele, ossifying fibroma of the maxilla, and fungal involvement. Of note, even the common cold can cause mucosal thickening of the sinuses sufficient to be seen on MRI. Elevations in ESR and C-reactive protein are independently predictive of sinusitis but are nonspecific. Recent clinical research from Johns Hopkins has raised the possibility of an underdiagnosed genetic predisposition for subclinical cystic fibrosis in some patients with symptoms of chronic sinusitis. A chromosome gene analysis of a buccal smear to look for the defect found in cystic fibrosis, followed by a sweat chloride test if indicated, may provide a diagnosis.
4. Treatment
Otolaryngologic consultation should be obtained. Endoscopic surgery should be considered when a 6-month trial of medical therapy has failed, or immediately in the case of a significant abnormality on imaging. With careful patient selection, endoscopic sinus surgery can achieve relief of pain in 56% of patients, and substantial improvement in a further 29%. Difficulties arise in patients with chronic sinus area pain that mimics sinusitis but may not be true sinusitis. When imaging repeatedly demonstrates normal sinuses, and there is a lack of any objective evidence for sinusitis, a multidisciplinary, multidimensional approach, including the specialties of neurology, psychiatry, and behavioral medicine, is required. These patients are unlikely to benefit from surgical intervention.
VI. TRIGEMINAL NEURALGIA
1. Diagnostic features
Trigeminal neuralgia is characterized by sudden, stabbing, severe unilateral facial pain in one of the three divisions (most frequently the second) of the trigeminal nerve. Onset is frequently triggered by mechanical stimulation such as talking, chewing, touch, or cold (e.g., cold wind). Attacks can last from several seconds to minutes. Periods of attacks can last weeks or months, followed by periods of remission of months or years. Carbamazepine responsiveness is considered a diagnostic feature.
2. Epidemiology
Incidence increases with age, peaking at 75 years, and thus more commonly presenting in women.
3. Diagnostic evaluation, imaging studies, and laboratory tests
MRI is an important diagnostic test for excluding intracranial masses and multiple sclerosis (MS), particularly in younger patients. MS should be considered in women younger than 30 years. An MRI can show demyelinating lesions of the white matter associated with MS. Symptoms such as diplopia, weakness, and clumsiness are suggestive of MS.
4. Treatment
Carbamazepine is the drug of first choice in treatment, with a beneficial response in more than 75% of patients. Its mechanism is depression of excitatory transmission in the brainstem trigeminal nucleus. Carbamazepine should be started at a dose of 200 mg daily and increased in increments of 200 mg until pain relief or side effects occur. The usual therapeutic dose range is 600 to 1,200 mg per day. Phenytoin is a less effective alternative but can be a useful adjunct to carbamazepine. Baclofen potentiates the action of carbamazepine at the trigeminal nucleus and can be a useful adjunct. It can be started at a dose of 30 mg daily, increasing to 50 to 60 mg daily. Gabapentin is a safe and well-tolerated adjunct to carbamazepine, titrated to effect from a starting dose of 300 mg at night to a usual range of 900 to 3,000 mg daily. Other agents used less frequently include tocainide, clonazepam, and sodium valproate.
Surgical approaches to the treatment of trigeminal neuralgia include microvascular decompression and radiofrequency electrocoagulation. Microvascular decompression relieves pulsatile compression of the trigeminal nerve at the cerebellopontine angle, achieving immediate pain relief in 79% and long-term relief in 73% of patients. Radiofrequency electrocoagulation is performed either by a percutaneous or open partial cranial rhizotomy, achieving immediate pain relief in more than 90% of patients. Unfortunately, this treatment is associated with pain recurrence in 80% of patients, occurring anytime from weeks to years after treatment. The key to a high success rate is ensuring that the patient fits a very rigorous definition for trigeminal neuralgia.
VII. BURNING MOUTH SYNDROME
1. Diagnostic features
Glossodynia is characterized by burning pain of the mucous membranes of the tongue (most commonly), mouth, hard palate, or lips. The onset of pain is gradual with no precipitating event, and it is usually bilateral. Associated symptoms are altered taste and dry mouth. Physical examination of the mouth is normal and excludes causes such as infection and trauma. Although nutritional and menopausal factors, abnormal glucose tolerance, and chronic mechanical irritation have all been suggested as causes, there is inadequate evidence to pinpoint these factors as the origin of burning mouth syndrome. Recent evidence suggests that peripheral nerve injury of the chorda tympani produces pain as a result of loss of inhibition of the trigeminal nerve.
2. Epidemiology
The prevalence rate is 1.5% to 2.5% in the general population. Patients are more likely to be female (3:1) and older than 50 years.
3. Diagnostic evaluation, imaging studies, and laboratory tests
There are no useful radiographic or laboratory examinations. As always, a careful history and physical examination are required to rule out other treatable causes.
4. Treatment
Fifty percent of patients experience spontaneous resolution within a variable length of time, up to several years after onset. Tricyclic antidepressants such as amitriptyline, nortriptyline, and desipramine (titrated in 10-mg increments to a range of 30 to 75 mg) and the serotonin reuptake inhibitor sertraline may be effective. In a study of 30 patients, clonazepam given at a dose of 0.5 to 1.5 mg daily lessened pain in 70% of patients; clonazepam was also found to be effective when applied topically to the mouth. A number of drugs including angiotensin-converting enzyme inhibitors and antihypertensives have been associated with burning mouth syndrome that is reversible with discontinuation of the drug. As pharmacologic therapy is unsuccessful in many patients, psychological support is important.
VIII. DEAFFERENTATION PAIN
1. Diagnostic features
Teeth and dental nerves are commonly amputated. Phantom tooth pain is similar to other phantom pain syndromes, producing pain in previously extracted teeth. Pain is constant with sharp exacerbations and is associated with local allodynia. Notably, sleep is undisturbed. The onset of pain can usually be related to a procedure such as dental extraction or sinus surgery.
2. Epidemiology
Phantom tooth pain prevalence rates of 3% closely match those of phantom pain following limb amputation (5%). Given the relative frequency of dental procedures when compared to limb amputation, phantom tooth pain is a common cause of facial pain. There is equal distribution between sexes, and although all ages are affected, occurrence in children is rare.
3. Diagnostic evaluation, imaging studies, and laboratory tests
Radiographs frequently demonstrate dental intervention but do not assist in diagnosis or management. History and physical exam are important as they pertain to extent of dental work and other trauma or surgeries in the area. History of prior severe dental pain of an extracted tooth or teeth, as well as prior sinusitis pain and traumatic pain, may suggest possible peripheral or central neuroplasticity.
4. Treatment
Pain therapies are targeted at both the central and peripheral components of deafferentation pain. The centrally acting drug of choice is gabapentin, starting at a dose of 300 mg at bedtime and increasing to a dose range of 900 to 3,000 mg daily. Some patients may be too sensitive, needing to start at 100 mg each evening and slowly titrate to higher doses. Other membrane-stabilizing agents such as carbamazepine and phenytoin are usually ineffective in phantom tooth pain, and efficacy of these agents suggests a diagnosis of trigeminal neuralgia. Clonazepam 1 to 3 mg daily and baclofen 30 to 60 mg daily are useful adjunctive agents. Amitriptyline and other TCAs, 10 to 75 mg daily, are effective, particularly when combined with a phenothiazine, such as perphenazine, in severe cases. A fixed daily dose of a narcotic agent such as oxycodone has been used successfully but is associated with a risk of dependence and addiction.
Peripherally acting agents include topically applied drugs and nerve blocks. Ketamine, capsaicin, and clonidine have been applied topically with mixed results. Nerve blocks with local anesthetic agents and low-dose steroids are effective but may require a number of trials to determine optimal injection sites for an individual patient. Surgical procedures are ineffective in treatment of phantom tooth pain and may actually increase pain severity.
IX. ACUTE AND POSTHERPETIC NEURALGIA
1. Diagnostic features
Acute herpetic neuralgia (AHN) arises as a result of herpes zoster infection (shingles) stimulating an acute inflammatory process of the dorsal root ganglion and peripheral nerves. Pain and cutaneous vesicles are located along the distribution of the affected peripheral nerve or nerves. Areas commonly affected are thoracic dermatomes (50%), ophthalmic division of the fifth cranial nerve (10% to 20%), and cervical dermatomes (10% to 20%). Shingles is almost always unilateral and may be recurrent (1% to 8%), usually in the same site.
Pain is described as burning, itching, well localized to the dermatome, with lancinating episodes, and it is associated with hyperesthesia and hyperalgesia. Intense lancinating pain and paresthesia usually diminish in the second or third week as the skin lesions begin to heal. In contrast, the pain of postherpetic neuralgia (PHN) is diffuse, dull, and aching, with a superficial dysesthetic sensation evoked by clothes or light touch. Pain persisting for longer than 1 month after complete healing of the acute herpes zoster lesions is considered PHN.
PHN is believed to result from deafferentation and hypersensitivity in the dorsal horn of the spinal cord. There is evidence that first-order neuron C-fiber death occurs both in the periphery and centrally in the substantia gelatinosa (lamina II) of the spinal cord. This may be followed by ingrowth of first-order neuron A-beta fibers from laminae III and IV into lamina II, which may explain the dysesthesia with normally non-noxious stimuli.
2. Epidemiology
PHN, ophthalmic involvement, and nervous system complications such as stroke, cranial neuropathy, and myelitis are associated with increasing age and an immunocompromised state.
3. Diagnostic evaluation, imaging studies, and laboratory tests
Diagnosis is clinical and based on the presence or history of vesicles, although complications such as stroke should be completely evaluated with CT or MRI.
4. Treatment
Early effective treatment of acute herpes zoster shortens the acute episode, decreases acute pain, and decreases the incidence of PHN. Antiviral therapy with acyclovir intravenous (IV) 5 mg/kg every 8 hours for 5 days, begun within 72 hours of the shingles eruption, is effective, and is particularly useful in immunocompromised individuals. The timely use of antiviral therapy has been shown to be effective in reducing both AHN and PHN. Amitriptyline, NSAIDs, doxepin, trazodone, and fluoxetine are useful for controlling the pain of AHN; if pain remains uncontrolled, narcotic agents can be added. Subcutaneous local anesthetic and steroid injections reduce acute and chronic symptoms but should be used with care in the immunocompromised patient.
TCAs are the mainstay of treatment in PHN. The efficacy of amitriptyline and desipramine has been confirmed in controlled clinical trials. Topical agents, such as a 5% lidocaine patch or salicylate prepared as 700 mg aspirin dissolved in 15 to 30 mL of chloroform or diethyl ether, can produce substantial pain relief with minimal systemic absorption. Anxiolytics and anticonvulsants have been used with less success. Narcotics should be reserved for patients who are unresponsive to other agents. Capsaicin is often poorly tolerated because of cutaneous sensitivity. A transcutaneous electrical nerve stimulator is associated with minimal morbidity and sometimes produces significant benefit; it is under utilized and should always be considered for patients with PHN.
X. PERIOCULAR PAIN
1. Diagnostic features
Ophthalmic pain results from stimulation of pain fibers related either directly or indirectly to the orbit. Cranial nerves involved may include the trigeminal, facial, vagus, and glossopharyngeal. The trigeminal sensory complex communicates actively with these cranial nerves, as well as the limbic and autonomic systems, and dips down to the level of C6. As a result, pain may be poorly localized, or it may be referred from other anatomic structures and areas with shared innervation peripherally and centrally. Pain can be classified as ocular, orbital, or referred.
Ocular pain
Corneal irritation or damage is associated with local pain, photophobia, and lacrimation, together with the sensation of a foreign body. Anterior scleritis presents with severe ocular pain, whereas posterior scleritis is characterized by less well defined orbital pain; either may be associated with a systemic collagen vascular disease. A triad of red eye, increased intraocular pressure, and a mid-dilated pupil is pathognomonic for acute angle glaucoma. Severe ocular pain is associated with headache, and it may radiate to the sinuses and teeth and be associated with systemic features such as nausea and vomiting. Atherosclerotic disease of the carotid may present with ocular ischemic pain. Uncorrected refractive error produces pain from excess ciliary body tone, pain that radiates to the head and brow. Photo-oculodynia is an uncommon pain syndrome of unknown cause in which ocular pain is precipitated by light.
Orbital pain
Orbital cellulitis presents acutely with pain exacerbated by palpation and movement. Orbital pseudotumor is an inflammatory process of unknown cause that presents with pain, chemosis, diplopia, and red eye. Trochleitis is characterized by orbital pain with movement, together with exquisite superonasal point tenderness. Retro-ocular pain and diminished vision are features of optic neuritis, which may occur alone or as a symptom of a demyelinating disease.
Referred pain
The proximity and convergence of afferent pain fibers produce referred pain. Direct and indirect noxious stimulation of the trigeminal nerve and its divisions produce primary and secondary trigeminal neuralgia. Occasionally, pain from the area of the greater occipital nerve radiates from the occiput to the eye and face (secondary trigeminal neuralgia), because of convergence and communication between the greater occipital nerve, C2, and C3, and the trigeminal sensory complex. Trigeminal neuralgia associated with a red eye, lacrimation, rhinorrhea, and Horner’s syndrome is known as Raeder’s syndrome. Cervical spondylitis may produce secondary trigeminal neuralgia presenting as orbital pain caused by the cervical branches in the spinal tract of the trigeminal nerve converging with the ophthalmic and maxillary divisions of the trigeminal nerve. Migrainous headache, sinusitis, otitis, mastoiditis, and dental pain can all be referred to the eye. Temporal arteritis presents with visual loss and ipsilateral facial pain and is diagnosed on temporal artery biopsy.
2. Epidemiology
Carotid occlusive disease, glaucoma, and temporal arteritis are more common in the elderly, whereas optic neuritis occurs predominantly in young adults, and MS with optic neuritis is seen in young to middle age adults.
3. Diagnostic evaluation, imaging studies, and laboratory tests
MRI is indicated to detect MS as a cause of optic neuritis. Raeder’s syndrome requires imaging to rule out a parasellar mass or carotid dissection as causes. Doppler flow studies are useful in detecting carotid stenosis as a cause of orbital ischemia. An ESR greater than 100 mm/hour, and increased C-reactive protein and fibrinogen levels are strongly associated with temporal arteritis.
4. Treatment
If temporal arteritis, optic neuritis, or orbital pseudotumor is suspected, high-dose corticosteroids should be started immediately (e.g., methylprednisolone 1g IV or prednisone 60 mg orally), and the patient should be referred to an ophthalmologist or a rheumatologist, depending on the suspected diagnosis. All patients with suspected eye pathology should be seen by an ophthalmologist. Keratitis and orbital cellulitis are treated aggressively with topical and systemic antibiotics, and with surgical drainage of collections and sinusitis as required. Acute-angle glaucoma requires urgent ophthalmologic referral and topical pupillary constriction, with or without laser iridotomy.
XI. PERIAURICULAR PAIN
1. Diagnostic features
Otitis media presents with either dull aching or sudden exquisite pain, with or without aural discharge, an inflamed tympanic membrane, and systemic evidence of infection (malaise and pyrexia). Otitis externa can be exquisitely painful, and it is generally an acute process. Mastoiditis and otitis pain may be referred to the eye, pharynx, and neck as a result of involvement of cranial nerve VII (supplying branches to both the eye and the ear), convergence with the trigeminal sensory complex, and the shared innervation of C2 and C3 and the petrous bone (Gradenigo’s syndrome). A common cause of otalgia that is frequently overlooked is referred myofascial pain from muscles of the neck, pharynx, and mastication.
2. Epidemiology
Otitis media presents more frequently in childhood and should always be considered in the immunocompromised patient. Mastoiditis and infected cholesteatoma are found more frequently in children and young to middle-aged adults.
3. Diagnostic evaluation, imaging studies, and laboratory tests
Elevated white cell count is supportive but nonspecific evidence of otitis media. CT and MRI are invaluable for mastoiditis and cholesteatoma. History and physical examination should direct an appropriate otolaryngologic referral.
4. Treatment
In general, urgent consultation with an otolaryngologist is required. Evidence of petrosal involvement requires broad-spectrum IV antibiotics. Referrals to a pain specialist are often from an otolaryngologist who has successfully treated the immediate pain problem, but the patient still suffers from chronic pain, together with frequent myofascial pain of the neck, head, and orofacial muscles. Treatment is multidimensional and comprehensive, covering possible neuropathic and nociceptive pain. Attention is directed to the common myofascial pains.
XII. HEAD AND NECK CANCER
1. Diagnostic features
Head and neck cancers present with a wide variety of symptoms. Frequently, a multidimensional approach is required during diagnosis, treatment, and recovery. Nociceptive and neuropathic pain may occur at any time during the course of disease and treatment, and coordination between surgical, dental, psychiatric, physical therapy, and oncologic consultations are frequently required.
Characteristic effects of the various manifestations of malignant disease and its treatment are as follows:

Local tumor growth and invasion results in local tissue destruction, secondary infection, nerve compression with mononeuropathy and plexopathy, secondary myofascial pain from distorted mouth opening and function, diplopia, and ptosis.

Surgical resection and reconstruction results in acute postoperative pain, nerve damage and resection, inadequate vascularization of myocutaneous flaps, and sacrifice of the accessory nerve.

Chemotherapy with vincristine and cisplatinum results in nerve damage and neuritis.

Radiotherapy results in mucositis of the gastrointestinal tract, osteoradionecrosis, cheilosis (tissue breakdown at the corners of the mouth), loss of salivary glands, secondary infection (fungal and bacterial), and loss of range of motion of the neck, facial and masticatory muscles (including limited mouth opening and remodeling of the TMJ, with secondary severe myofascial pain and dysfunction).

Nutritional deficiencies (secondary to pain, loss of appetite, poor caloric intake, and mismatch between metabolic demands and intake) result in poor fit of dental prostheses (with or without pain) and in pyridoxine, B12, and other specific vitamin and mineral deficiencies.

Secondary infection results in tissue breakdown and pain.

Psychosocial factors contribute to the overall pain response inducing fear, anxiety, lack of self esteem; there are also cosmetic concerns, and fears of tumor recurrence lead to patients’ misinterpreting symptoms as tumor recurrence rather than the expected secondary complications of therapies.
2. Epidemiology
Head and neck cancer occurs predominantly in older adults, although lymphoma, adenocarcinoma of the sinuses, and squamous cell carcinoma do occur in younger adults. Smoking and chewing of tobacco; alcohol; chronic irritation and injury of the intraoral mucosa secondary to habits, damaged dentition, and poorly fitting fixed and removable prostheses; and sun exposure and fair skin are strongly associated with the development of head and neck cancers.
3. Diagnostic evaluation, imaging studies, and laboratory tests
Radiologic imaging techniques of CT and MRI, endoscopy, biopsy, and surveillance are invaluable in the management of head and neck cancer.
4. Treatment
Pain due to head and neck cancers should be treated following the same principles as those outlined in Chapter 32. With particular reference to head and neck cancer, physical therapy can improve range of motion of the neck, mouth, and TMJ. Myofascial pain of the shoulders, neck, and head, and headache are frequent secondary occurrences and may also respond to physical therapy. Nutritional consultation may be helpful, as may dental consultation to aid with oral function and cosmesis.
XIII. CONCLUSION
Facial pain has a vast number of complex causes, and its successful treatment requires contributions from many different specialties. This pain is one of the most distressing of all painful syndromes and warrants aggressive and appropriate treatment in a multidisciplinary setting. This chapter outlines some of the causes, diagnostic features, and treatments of facial pain.
SELECTED READINGS

1.
Acquadro MA. Headache and sinusitis. Curr Opin Otolaryngol Head Neck Surg 1998;6:2–5.

2.
Barker FG 2nd, Jannetta PJ, Bissonette DJ, et al. The long term outcome of microvascular decompression for trigeminal neuralgia. N Engl J Med 1996;334:1077–1083.

3.
Bohr TW. Fibromyalgia syndrome and myofascial pain syndrome: do they exist? Neurol Clin 1995;13:365–384.

4.
Graff-Radford SB. Facial pain. Curr Opin Neurol 2000;13:291–296.

5.
Hu JW, Tsaj CM, Bakke M, et al. Deep craniofacial pain: Involvement of the trigeminal subnucleus caudalis and its modulation. In: Jensen TS, Turner JA, Wiesenfeld-Hallin Z, eds. Proceedings of the Eighth World Congress. Seattle: IASP Press, 1997;497–506.

6.
Huang W, Tothe MJ, Grant-Kels JM. The burning mouth syndrome. J Am Acad Dermatol 1996;34:91–98.

7.
Marbach JJ. Medically unexplained chronic orofacial pain: Temporomandibular pain and dysfunction syndrome, orofacial phantom pain, burning mouth syndrome and trigeminal neuralgia. Med Clin North Am 1999;83:691–710.

8.
Marbach JJ. Orofacial phantom pain: theory and phenomenology. J Am Dental Assoc 1996;127:221–229.

9.
Marbach JJ, Lennon MC, Link BG, et al. Losing face: Sources of stigma as perceived by chronic facial pain patients. J Behav Med 1990;13:583–604.

10.
Merrill RL. Orofacial pain mechanics and their clinical application. Dent Clin North Am 1997;41:167–187.

11.
Truelove E, Sommers E, LeResche L, et al. Clinical diagnostic criteria for TMD. J Am Dent Assoc 1992;123:47–5

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