--------------------------------------------------------------------------- TITLE: Headache and Facial Pain SOURCE: Dept. of Otolaryngology, UTMB, Grand Rounds DATE: 20 February 1991 RESIDENT PHYSICIAN: Joseph J. Bradfield, M.D. FACULTY: Francis B. Quinn, Jr., M.D. DATABASE ADMINISTRATOR: Melinda McCracken, M.S. --------------------------------------------------------------------------- "This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion." I. ANATOMY A. Study of the causes and treatment of headache presupposes a knowledge of the pain sensitive structures and pathways for pain mediation in the head and neck. B. Pain sensitive cranial structures include: 1. Skin, scalp, fascia, muscles and extracranial blood vessels. 2. Parts of the dura at the base of the brain, and the dural sinuses. 3. Dural arteries. 4. Arteries at the base of the brain, and their larger tributaries. 5. Cervical nerves C2 and C3. C. Pain insensitive structures: 1. Skull (periosteum slightly sensitive). 2. Brain parenchyma 3. Pia, arachnoid, and some dura mater. 4. Ependymal lining of the ventricles. 5. Choroid plexus. D. Sensory information concerning head and neck pain is carried by cranial nerves V (trigeminal), IX (glossopharyngeal), and X (vagus), and by the first through third cervical nerves. 1. The trigeminal nerve arises in the pons and forms the gasserian ganglion. It then divides into three branches - ophthalmic, maxillary and mandibular. a. The ophthalmic division passes through the lateral wall of the cavernous sinus , giving branches to the meninges. It divides into the lacrimal (sensory for the lateral eyelid and conjunctiva), frontal (scalp, medial eyelid and conjunctiva),and nasociliary (dorsum of nose and septum) branches. b. The maxillary division passes through the cavernous sinus, the through the foramen rotundum to the infraorbital canal and foramen. Its terminal branches include the meningeal, pterygopalatine (palate), posterior superior nasal (nasal cavity) and superior alveolar (maxillary teeth). c. The mandibular division passes through the foramen ovale. It gives off a meningeal branch, then branches anteriorly to the muscles of mastication and buccal nerve (corner of mouth and buccal mucosa). A posterior branch divides into the lingual (anterior 2/3 of the tongue), inferior alveolar (mandibular teeth and chin), and auriculotemporal (ear and scalp). 2. The glossopharyngeal nerve and the vagus receive sensory input from the posterior tongue, naso-, oro, and laryngopharynx, middle ear, and posterior cranial fossa. D. Intracranial structures above the tentorium are supplied by branches of the trigeminal nerve, while intracranial structures below the tentorium are supplied by the glossopharyngeal, vagus, and upper cervical nerve roots. Pain due to intracranial lesions may be referred to the area of the head and neck served by the involved nerve, giving a clue to the location of the lesion, but parenchymal lesions may exist that because of their location not affect a pain sensitive structure and may be therefor asymptomatic. E. In general, the location of pain in the head and neck is a good indicator of the location of the pathology. Exceptions to this rule include pain arising from the posterior half of the sagittal sinus and the transverse sinus which is referred to the ipsilateral eye and forehead; pain from the middle meningeal and middle cerebral arteries is referred behind the eyes; pain from the carotid bifurcation is referred to the scalp, ear nose teeth tongue and face; and pain from the internal carotid artery is felt deep in the eye or ear. II. HISTORY AND PHYSICAL EXAMINATION A. History - The majority of head and neck pain patients have normal physical examinations. Therefor a detailed and accurate history is the single most important factor in making a correct diagnosis. Further, it may be benificial to have the patient keep a chart of headache frequency for several months to assist in diagnosis. Specific areas to address in the history: 1. Onset - including time of life headaches began, a significant life event that occurred prior to onset, and the specific time of day when headache strikes. 2. Location - unilateral or bilateral, localized or generalized. 3. Frequency - including seasonality. 4. Duration. 5. Severity. 6. Characteristics of the pain - throbbing, pulsating, burning, etc. 7. Any associated prodrome. 8. Associated symptoms - photophobia, sonophobia, nausea, vomiting, lacrimation, nasal congestion. 9. Sleep habits - delayed sleep, early awakenings, does the headache awaken the patient. 10. Precipitating factors - fatigue, loss of sleep, stress, menses, sunlight, foods. 11. Occupation - job stress, chemical or biological substance exposure. 12. Family history - if one parent suffers migraines, there is a 45% chance of a child being affected. Increases to 70% if both parents are afflicted. 13. Gynecologic - galactorrhea, amenorrhea, relation to menses, hormone supplementation. 14. Medical history - trauma, seizures, surgeries. 15. Systems review. 16. Allergy. 17. Previous headache workups. 18. Medications. B. Physical Examination - will most often be normal, but may provide specific diagnostic information. Divided into four areas. 1. The general survey includes observation of the body habitus, general appearance, general behavior, and facial characteristics, as well as a general physical examination. 2. A brief mental status exam will provide clues regarding depression, anxiety, agitiation, or memory impairment. 3. A careful head and neck exam with attention to trigger points, local inflammation or infection, TMJ pain, sinus pain, carotid artery pain or bruits, or muscle spasms. 4. A careful neurological examination. This should include the cerebellar, motor and sensory examination, as well as a thourough examination of the cranial nerves. Special attention should be paid to II,III,IV, and VI since they are often involved in pathologic processes. III. CLASSIFICATION OF HEADACHE AND FACIAL PAIN A. Due to the clinical diversity of headache and facial pain syndromes, it has been difficult to devise an acceptable classification system. B. Headaches are generally classified by etiology: 1. Vascular - migraines, cluster headache, toxic vascular headache, hypertension. 2. Muscle contraction - stress and cervical osteoarthritis. 3. Traction and inflammatory - neoplasia, infection, granulomatous disease, collagen vascular disease, etc. C. Facial pain is generally classified by location: 1. Ophthalmic pain. 2. Nasal and sinus pain. 3. Dental pain. 4. Neuralgias. 5. Causalgia. 6. Atypical Facial Pain. IV. SPECIFIC TYPES OF HEADACHE A. Vascular Headaches - Certain characteristics which are associated with vascular headaches include recurrent attacks of varying severity with interposed symptom free intervals. The pain is usually throbbing, unilateral, and may vary from side to side. Anorexia, nausea, vomiting, vertigo, tinnitus, photophobia, sonophobia, autonomic disturbances and a positive family history are frequently noted. 1. Migraine Headaches - the pathophysiology of migraine headache continues to be debated. The prevailing view has been that migraine is primarily a biochemical/ vascular disorder. This theory holds that after an initial period of vasoconstriction and tissue ischemia (corresponding to the prodrome) there is subsequent vasodilatation with release of nocicepter stimulating substances (bradykinins, histamine, prostaglandins and serotonin) which results in headache. Considerable evidence in favor of this theory as well as opposed to it has accumulated. Others believe the underlying pathology is neurologic in origin, with the vascular changes merely epiphenomena. Migraines are further divided into the following types: a. Classic Migraine (10 - 30%) - The presence of a sharply defined neurological prodrome that precedes, overlaps or accompanies the headache defines the classic migraine. The prodrome is usually visual (80%), but may be sensory or motor, and include paresthesias (30 - 66%), dizziness (30%), dysphasia, nausea, vomiting and hemiparesis. Other clinical data: i. Onset during puberty or adolescence. ii. Less severe after age 40. iii. Pain less severe and shorter than common migraines. iv. Pregnancy may increase frequency. v. Acute sensory stimuli may trigger attacks. b. Common Migraine ( 80 - 90%) - These headaches lack a well defined prodrome, but may be preceded by a vague, often prolonged prodrome such as mood changes, fatigue, depression, or euphoria. Associated symptoms include nausea, photophobia, sonophobia, dizziness or blurred vision. Other clinical data: i. Headache may last for hours or days. ii. May be unilateral or bilateral. iii. May be throbbing and accompanied by scalp tenderness. iv. Strikes on the downslope of the stress curve. v. May be precipitated by stress, fatigue, loss of sleep hypoglycemia and certain foods. vi. Past history of travel sickness, fainting or other autonomic dysfunction is common. c. Complicated Migraine (2%) - This group of disorders is characterized by the persistence of a focal neurological defect after the headache has resolved. Three varieties are generally included. i. Ophthalmoplegic Migraine - a rare form that occurs in children or young adults. Ophthalmoplegia develops toward the end of a bout of periorbital pain, manifesting as diplopia, ptosis, strabismus and meiosis. The headache tends to clear in hours to days, with the ophthalmoplegia lasting days to weeks, usually with full recovery. Tumor, aneurysm, infarction or Tolsa-Hunt syndrome may mimic this disorder, and a normal CT scan confirms the diagnosis. ii. Hemiplegic Migraine - usually affects children and adolescents with a family history of migraine. Hemiparesis occurs followed in 10 - 60 minutes by headache. The hemiparesis may persist for days to weeks after headache resolves, but full recovery is the rule. iii. Ophthalmic Migraine - refers to the persistence of a visual defect which is usually monocular or hemianopic. The disorder must be differentiated from amaurosis fugax by the lengthy time course, hemianopia, and presence of headache. c. Facial Migraines - this syndrome has all the findings of migraine headache, but the pain is localized to the lower half of the face. It is necessary to distinguish facial migraines from other causes of facial pain. d. Migraine equivalents - defined as any of the symptom complex usually associated with a migraine disorder, but without the headache. Usually occurs in those with a history of migraine, and is a diagnosis of exclusion. e. Treatment of migraine headaches is based both on prophylaxis and symptomatic treatment. It is also important to counsel the patient regarding the disease, with emphasis on the lack of permanent damage. Symptomatic treatment includes: i. Rest. Sleep will often abort an attack. ii. Metaclopramide 10 mg prn nausea. iii. Ergotamine 1-2 mg q30' up to 6 mg per attack and 12 mg per week. iv. Dihydroergotamine may be used parenterally. v. Ergotamines are contraindicated in peripheral vascular disease, hypertension, hyperthyroidism or ischemic heart disease. Prophylactic treatment includes: i. Avoidance of precipitating factors. ii. Propranolol 80 - 160 mg per day iii. Methysergide maleate beneficial in over 50%. iv. Cyproheptidine. v. Amitriptyline at lower than antidepressant doses. vi. Calcium channel blockers have shown promise, but are not widely used. 2. Cluster Headaches - An uncommon type of headache that afflicts young adult men. There is usually no family history. The attacks consist of excruciatingly severe, constant, unilateral pain invading the orbit, face and temple. They last 10 minutes to two hours and may occur one to three times a day. Patients may manifest agitated behavior and pacing. Frequently there is associated stuffiness, rhinorrhea, lacrimation, and flushing. Up to 40% may develop an incomplete Horner's Syndrome (anhidrosis is absent). Other clinical data: a. Attacks come in clusters lasting weeks to months, with intervening symptom free intervals. b. Attacks commonly awaken the patient from sleep and occur at the same time every day. c. Attacks may be precipitated by vasodilators, alcohol, high altitude or lack of sleep. d. A variant of cluster headaches is Chronic Paroxysmal Hemicrania. It differs from clusters in that the pain lasts minutes, occurs many times per day and responds to indomethacin. e. Treatment of cluster headaches is also both symptomatic and prophylactic. i. 100% Oxygen for 15 minutes aborts headache in 80% of patients. ii. Ergotamine aerosol may decrease the severity. iii. Ergotamine, methysergide or prednisone may be helpful for prophylaxis during the cluster period. 3. Systemic and Toxic Vascular Headaches - a number of specific systemic and toxic causes for headache are recognized. Toxic vascular headache are characterized by bilateral throbbing headache. The majority of the expiremental evidence suggests the cause is dilatation of the cephalic vasculature. a. Hypertension with diastolic pressures in excess of 130 mm hg. Up to 80% of those with pheochromocytoma report headaches. b. Systemic lupus erythematosis causes noninflammatory changes in small vessels in the CNS which may lead to hemmorrhage and microinfarcts. c. Vasodilators are frequently found in foods. Specific offenders are MSG (Chinese Restaurant Syndrome); tyramine which is found in cheeses, wines and fermented beverages among other things; and nitrites (hot dog headache). d. Other causes of vasodilatory headaches include infection and fever, hypoxia, hangover, postseizure status, ice cream ingestion, caffeine withdrawal, and orgasm. B. Muscle Contraction Headache - is characterized by a steady non-pulsatile ache which may be localized or generalized. The most common type of head and neck pain, it is estimated that 80% of the population suffers from this type of headache at some point. Typically there is a hatband distribution of tenderness, and palpable tender nodules or trigger points. Emotional factors are of prime significance in this type of headache, and effort should be made to ascertain the underlying causes. 1. The headache caused by cervical spondylosis and cervical arthritis is a subset of muscle contraction headaches. It is felt the etiology is the entrapment of the upper cervical nerve roots in spasming nuchal musculature. 2. Physical exam of the patient with cervical arthritis will usually disclose spasm of the neck muscles, tenderness, and limitation of motion. C. Traction and Inflammatory Headache - results from the impingement on, invasion or stretching of the pain sensitive structures of the head, usually blood vessels.This may be from tumor, other space occupying lesions, or from other causes of increased intracranial pressure. Lumbar puncture with CSF leakage may result in headache lasting from 2 weeks to 4 months. Immunologic disease and arteritides result in headache by causing inflammation of pain sensitive structures - most often arteries - both intra- and extracranially. Examples include polyarteritis nodosa and temporal arteritis. V. SPECIFIC TYPES OF FACIAL PAIN A. Ophthalmic Pain - From am ophthalmological point of view, eye pain may be divided into three categories - eye pain without ocular findings, eye pain with ocular findings, pain associated with non-ocular etiologies that may involve the eye. 1. Eye pain without ocular findings is most often due to the optical error of the eye. Asthenopias result when the eye's attempts at accomodation are frustrated either through the stiffness of the lens, conflicting impulses regarding accomodation and convergence, muscle imbalance or convergence insufficiency (the inability to maintain convergence at 14 inches). The result is muscle strain, fatigue and pain. Symptoms are usually less in the morning and worsen through the day. Treatment is the provision of appropriate corrective lenses. 2. The diagnosis of eye pain associated with ocular findings is usually much more straightforward. Common etiologies include zoster infection, blepharitis, corneal abrasion, acute angle closure glaucoma, uveitis, and optic neuritis. Diseases of the periorbital soft tissues such as hyperthyroidism, infection, or other inflammation may be causal. B. Nasal and Sinus Pain - Numerous pathologic entities may cause nasal and sinus pain. Of these, the most common cause of facial pain is sinusitis. Fortunately the diagnosis of acute sinusitis is usually straightforward. However, chronic sinus disease may be more difficult to diagnose. Sinus disease may be a cause of headache even when not suspected from case history. 1. The typical triad of chronic sinusitis is nasal congestion, pathologic secretion and headache. Headache is a variable finding and is uncommon in children less than five. 2. The pattern of referred sinus pain has been well documented. Wolff studied 25 subjects with various disorders by stimulating the nose and paranasal sinuses with probes, DC current, and epinephrine pledgets. He found: a. Pain from the pharynx, nasopharynx and eustachean tube was referred to the skin over the hyoid and stretching back to the ear. b. Pain from the middle part of the septum was referred to the zygoma, and from the ethmoid portion to the medial and lateral canthi. c. Pain from stimulation of the inferior turbinate is referred to the maxilla and the maxillary teeth, from the middle turbinate to the zygoma, and from the superior turbinate to the medial canthal region. d. Stimulation of the maxillary antrum resulted in lacrimation, injection of the ipsilateral eye, and pain referred to back teeth, nasopharynx, zygoma and temple. e. Stimulation of the nasofrontal recess also results in lacrimation and injection, as well the pain in the inner canthus, zygoma and temple. f. Pain from the frontal sinus is referred directly over the sinus. g. The anterior ethmoids refer pain deep between the eyes and in the periorbital area. Posterior ethmoid stimulation produced pain in the lateral maxillary teeth and the lateral canthal region. h. Pain from the sphenoid sinus radiated to the vertex. i. Stimulation of the maxillary sinus resulted in pain in the upper teeth, around the eye, and over the sinus. 2. Since sinusitis is not usually confined to one sinus, referred headache patterns may involve multiple branches of the trigeminal nerve. 3. The same anatomic variations that predispose to recurrent sinusitis also predispose to headaches: a. Septal spurs and deviations. b. Agger nasi cells c. Variations of the uncinate process. d. Concha bullosa. e. Paradoxically bent turbinates. f. Variations of the ethmoid bulla. 4. Nasal endoscopy and CT scanning are valuable tools in the identification of these abnormalities. Once identified, the patient may benefit greatly from simple endoscopic correction of these abnormalties. 5. Other causes of nasal and sinus pain include: a. Other inflammatory conditions such as: i. Rhinoscleroma ii. Granulomatous conditions are usually not painful unless superinfected. iii. Allergic Rhinitis. iv. Rhinitis medicamentosa, including cocaine abuse. v. Wegeners granulomatosis. b. Malignancy. i. Cancer of the sinuses is uncommon. ii. Squamous cancer of the maxillary sinus is the most common. c. Trauma, including septal hematoma. C. Dental Pain - The diagnosis of acute dental pain is usually straightforward. Disorders of the TMJ, however present a challenging diagnostic problem. 1. Two theories of TMJ pain exist. a. One theory is that occlusal problems lead to muscle dysfunction, spasm, pain and articular problems. b. Others believe the underlying problem is muscle hyperactivity caused by stress, bruxism. They believe dentition is not the cause, but a predisposing factor. 2. TMJ may present with pain, muscle tenderness, popping, clicking, limitation of movement or otologic manifestation. Specific triggering factors may be noted. 3. More than 75% of patients respond to heat, muscle relaxants and analgesics. D. Neuralgias - Criteria for a true neuralgia include a paroxysmal usually stabbing pain in the known distribution of a cranial or spinal nerve; the pain is usually measured in seconds, although there may be an underlying ache; there is a specific trigger zone; and there is no objective sensory or motor loss in the distribution of the nerve. Trigeminal and vagoglossopharyngeal neuralgias are true neuralgias. The remainder are classified as other neuralgias. 1. Trigeminal Neuralgia - Characterized by a recurrent sharp, stabbing, unilateral pain in the distribution of one of the trigeminal branches - most often V2. Pain is usually triggered by innocuous stimulus somewhere in the distribution of the affected nerve. a. An estimated 10000 Americans develop trigeminal neuralgia each year. b. Onset is rarely before age 35. c. The right side is more commonly involved. d. Physical examination is normal. e. Trigeminal neuralgia may be secondary to multiple sclerosis, tumor, aneurysm,congenital anomaly, vascular compression or idiopathic. f. 80 % of patients respond to treatment with carbamazepine. Baclofen, clonazepam and dilantin have also been used with less success. Surgical treatment usually involves destruction of the trigeminal nerve roots or Gasserian ganglion, either by direct visualization or more recently by injection with glycerol - which tends to damage pain mediating fibers selectively. 2. Vagoglossopharyngeal Neuralgia - Is characterized by a sharp, lancinating pain originating in the throat or ear and radiating to other areas in the sensory distribution of CN IX and X. A positive cocaine test in a known trigger zone confirms the diagnosis. a. Vagoglossopharyngeal neuralgia is exceedingly rare. b. Trigger points are usually in the posterior pharynx. c. Most often presents over age 40. d. May be accompanied by bradycardia, syncope and convulsions. e. Medical treatment less satisfactory than trigeminal neuralgia. Carbamazepine effective in about 20%. Surgical treatment involves sectioning the IX nerve and the upper roots of the X nerve, but has a high incidence of post operative complications. 3. Geniculate Neuralgia - originally described by J. Ramsay Hunt, is a sharp, stabbing pain in the internal or middle ear, the eustachean tube or mastoid. It may, however take the form of a sharp pain superimposed on a dull ache. a. Trigger points are usually not present. b. A search for vesicles should be made. c. Carcinoma of the nasopharynx or external auditory canal must be excluded. d. There are no reports of successful medical therapy. 4. Postherpetic Neuralgia -is a disease of the elderly, with 90% of the cases occurring after age 60. It is a sharp, stabbing ache in the involved area following about of zoster. a. V1 branch is most commonly affected. b. Treatment of zoster in the over 50 age group should aim also at reducing postherpetic pain. Local infiltration, sympathetic nerve blocks and acyclovir should be considered. c. Some studies suggest prednisone may significantly reduce the period of postherpetic pain. 5. Sphenopalatine Neuralgia - or Sluder's neuralgia is characterized by a constant burning or aching sensation behind the eyes or in the area of the hard or soft palate. Episodes may follow a dental or sinus infection and may be associated with conjunctival injection, lacrimation and facial erythema. a. Females are more commonly affected 2:1. b. Most common between age 30 - 50. c. May be differentiated from cluster headaches by history. d. Attacks may be precipitated by drafts, climatic change, alcohol, or tobacco. e. Cocaine block of the sphenopalatine ganglion may be both diagnostic and therapeutic. 6. Occipital Neuralgia - is classified as primary or secondary. The primary type is a true neuralgia and is associated with severe pain in the distribution of the greater and lesser occipital nerves. Definite trigger finding are present, and there is no demonstrable neurologic deficit. The secondary type is more persistent dull ache and is associated with the Arnold- Chiari malformation, tumor, cervical spondylosis, and subgaleal trauma. a. Treatment of the primary type is initially with tricyclics, but local nerve blocks or steroid injections may cause cessation of the attacks. b. Treatment of the secondary type is the treatment of the underlying disorder. 7. Raeder's Paratrigeminal Syndrome - consists of a throbbing headache in the upper maxillary or ophthalmic branches of the trigeminal nerve. In addition there is a partial Horner's syndrome on the afflicted side (no anhidrosis). Divided into two groups based on involvement of other parasellar cranial nerves. a. Group I patients have other parasellar nerve involvement. Associated conditions include tumor, infection or trauma of the petrous apex, and calcifications of the internal carotid artery. b. Group II patients lack this involvement and tend to be associated with upper respiratory infections, sinusitis and otitis media, dental abscesses, hypertension,and internal carotid aneurysms. c. 90% of cases involve males. d. The left side is more frequently affected 2:1. e. Group I patients are treated by treating the underlying process. f. Group two patients are often self limited, but may benefit from amitriptylene. 8. Carotidynia - is a syndrome of swelling and tenderness of the carotid artery, with pain in a variable distribution, but usually referred deep into the face. a. This syndrome may actually be related to migraine syndromes, and responds to migraine medication. b. Many patients also respond to non-steroidals. E. Causalgia (Reflex Sympathetic Dystrophy) - Characterized by a burning, searing pain out of proportion with the inciting trauma or clinical appearance. 1. Reported as a sequela of trauma, surgery, difficult dental work, or head injury. 2. Localized heat, redness and pain have been noted, although usually not the trophic changes seen in the extremities. 3. Pain precipitated or increased by local stimulation or stress. 4. Stellate ganglion blockade may give symptomatic improvement. Cervical sympathectomy has been performed where blockade has given only temporary relief. F. Atypical Facial Pain - Includes those patients in whom structural pathology or other causes of head and neck pain have been ruled out. 1. Generally middle aged women. 2. Pain is usually aching and diffuse, and does not correspond with neuroanatomy. No trigger points or precipitating factors are found. 3. Pain is of variable intensity and duration. 4. Depressive, neurotic, or hysterical features are prominent. 5. There are frequently GI complaints, dizziness, and fainting. 6. Most have had a variety of dental or otolaryngologic procedures and evaluations. 7. The role of psychogenic factors may be evaluated with the "MADISON" scale developed by Hackett. Each of the following is rated on a scale from 0 to 4, where a total score above 15 suggests the need for psychiatric intervention. M - Multiplicity of pain location and variety. A - Authenticity (The patient wants the doctor to believe his pain is real). D - Denial of emotional difficulties I - Interpersonal relationships are disturbed. S - Singular pain separates patient from all others. O - "Only you can help". N - Nothing has worked before. 8. Most respond to antidepressants. VI. CONCLUSION A. Dealing with the patient with headache and facial pain, can be both very challenging and very trying for the otolaryngologist. 1. Diagnosis may be difficult. 2. Many of these disorders are chronic and will require long term attention, without significant improvement. B. In dealing with the chronic pain patient it is important to set realistic goals. 1. Patient counseling is important. 2. A reasonable goal is probably a 50% reduction in the patients symptoms: a. A 50% reduction in pain. b. A 50% increase in function. c. A 50% decrease in medications. C. A multimodal approach should be used, including: 1. Medications. 2. Diagnostic and therapeutic nerve blocks. 3. Physical therapy - including home exercise. 4. Stimulation produced analgesia such as TENS 5. Psychological techniques including behavior modification, relaxation, and biofeedback. 6. Social and vocational rehabilitation. ----------------------------------------------------------------------- BIBLIOGRAPHY 1. 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