Pain

Current Concepts in Pain Management

Steven B. Graff-Radford, DDS

Copyright 2003 Journal of the California Dental Association.

Author

Steven B. Graff-Radford, DDS, is co-director of the Pain Center and an adjunct associate professor at UCLA School of Dentistry.

The majority of people afflicted with orofacial pain have acute pain that resolves quickly, but some are left with chronic and disabling pain. Therapy must be provided to deal with the nociception, behavior, and suffering. Appropriate behavioral evaluation may be required prior to developing a treatment plan. The treatment should then be carefully outlined and presented in a treatment-planning visit and may include physical, pharmacologic, and behavioral aspects.

Orofacial pain is the result of a complex interaction of nociception, pain, suffering, and behavior that afflicts millions. The majority of people afflicted with orofacial pain have acute pain that resolves quickly, but some are left with chronic and disabling pain. Too often, this chronic pain is left undiagnosed; and patients continue to suffer. Because dental schools teach little about chronic pain, a diagnosis is infrequently made; or patients with non-odontogenic pain -- e.g., migraine, cluster headache, trigeminal neuralgia, or myofascial pain -- are misdiagnosed. The term “atypical” is often suggested to categorize the pain and implies a psychiatric or behavioral problem.1 “Idiopathic,” when referring to a medical problem, suggests there is something unknown and does not define the problem. The same applies to terms incorporating the word “atypical.” It has been reported that patients described as atypical or idiopathic can be diagnosed if evaluated by someone with more experience.2 The International Association for the Study of Pain3 and the International Headache Society4 take the position that there are better terms for facial pain diagnoses than atypical or idiopathic.

The term “idiopathic facial pain” has included diagnoses such as atypical facial pain, atypical odontalgia, masticatory muscle disorders, and traumatic neuralgia. These categories serve to perpetuate the limited knowledge of orofacial pain where the etiology is unclear. The most comprehensive facial pain classification to date incorporates the International Headache Society criteria and expands it to include disorders that were not clearly defined.4 It is suggested that if the clinician does not know what is causing the pain, the term “idiopathic” or “pain of unknown origin” be used. The patient should then be referred for better diagnosis. The major categories of pain are intracranial, extracranial, musculoskeletal, neurovascular, neuropathic, and psychogenic. In many categories, the etiologic mechanism, peripheral and/or central, is poorly understood. Pain disorders must be classified based on an understanding of the underlying mechanism, etiology, and clinical presentation. It is also necessary to recognize the differences in acute and chronic pain because treatment approaches are different.5

Acute pain may best be described as a useful pain, e.g., acute pulpitis, mucosal irritation secondary to a prosthesis, and active infection. It is the essential component that allows the sufferer and his or her practitioner to know something is wrong. It usually lasts a predictable time. If the duration extends beyond what is expected, further investigation is needed; or a chronic etiology may be expected. There is little difficulty in defining the specific pathology (e.g., denture irritation) of acute pain; and therapy is usually obvious (e.g., removal of irritating source). Chronic pain typically begins with an acute episode and progresses to a chronic condition if it is inappropriately managed, no treatment is sought, or treatment was not completed, e.g., a peripheral neuropathic pain may develop following a herpes infection that causes acute pain. The pain duration is usually defined as being longer than six months. The pain is not necessarily useful and is frequently associated with increased anxiety and depression, possibly because numerous doctors have been seen and numerous procedures tried without mitigation of the pain.

Management Approaches for Chronic Pain

A practitioner must carefully assess and diagnose the pain before developing a therapy. Treatment should be aimed at a specific diagnosis or pain mechanism. Using poorly defined diagnoses such as atypical trigeminal neuralgia or atypical facial pain should be avoided. If a practitioner cannot make an accurate diagnosis, he or she should consider referring the patient. The dentist must try to understand each component of the chronic condition so a comprehensive and structured therapy can be offered. Therapy must be provided to deal with the nociception, behavior, and suffering. Appropriate behavioral evaluation may be required prior to developing a treatment plan. The treatment should then be carefully outlined and presented in a treatment-planning visit. Treatment may include physical, pharmacologic, and behavioral aspects. Using a structured treatment agreement is helpful in explaining therapy to patients.

Treatment Planning

A treatment contract is a written agreement between a patient and health care provider.6 This is imperative in a setting such as a chronic pain center where patients receive simultaneous treatment from multiple specialists. In clinical practice, using this concept helps to prevent patients who are not responding from being overtreated. Patients who suffer from chronic disease often feel a loss of self-control. Too often, they have been given the false promise that the next surgery, medication, or alternative therapy will “cure” the problem, only to be disappointed. It is therefore recommended that a treatment contract be used to provide clear treatment explanations, set treatment goals, set treatment duration, define the patient’s and health care providers’ responsibilities, and provide specific contingencies to enhance compliance.

When providing a treatment explanation, it is suggested that all treatment possibilities be discussed. Where possible, this should be provided in stages, especially if one component of therapy is contingent upon the success of another. It is recommended that all possible therapies be outlined, allowing flexibility to change to alternative plans if the first choice is not working out. Once a treatment program is established, the treatment contract will help ensure compliance. Additionally, if the patient and clinician sign the treatment contract, the full course of treatment is agreed upon, preventing the patient from dictating changes.

Setting goals is important in a treatment contract. It is recommended that the treatment goals be stated as behaviors (process goals) to be learned, increased, decreased, or eliminated, rather than specific percentage reductions in pain (end goals). The goals need to be realistic and attainable.

Setting treatment duration is useful in allowing specific therapies to be tested prior to re-evaluating and moving forward with alternatives or proceeding with further workup. The treatment contract should specify therapy duration and frequency. In patients for whom noncompliance or tardiness is a possibility, consequences may include stopping therapy or referring the patient for inpatient care. By agreeing to a treatment contract that sets a time limit, the patient is made aware that there is a treatment constraint. Therefore, there is a consequence if he or she misses appointments or does not follow the instructions outlined.

Sharing responsibility for treatment outcome is especially important in chronic pain patients. It is not uncommon for the patients’ expectation to be unrealistic. In chronic migraine, it is not possible to “cure” the pain. Migraine is a genetic disorder that at this time can only be managed. Therefore, a treatment contract will define what the patient needs to do to manage the pain as opposed to what the clinician can do for the patient. Pain management usually requires a multidisciplinary approach. Patients who are exposed to more than one clinician are apt to receive conflicting information or may conveniently interpret information as conflicting to split the team. The treatment contract enables one person, “the pain manager,” to coordinate the treatment team. All questions or problems should be discussed with the pain manager. The entire team, including the referring physician and pharmacy, should have a copy of the treatment contract to prevent miscommunication.

The treatment contract can be used to define contingencies. Behaviors that are required and prohibited should be specified. These may include issues related to missed appointments, late arrival, medication usage (decreasing dose schedule, time contingent administration vs. pain contingent administration), noncompliance, and home program. The consequences of undesirable behaviors should be clearly spelled out.

Therapies

Orofacial pain may be addressed with a variety of physical, pharmacologic, and behavioral strategies. Therapy principles and rationales will be discussed, rather than disease-specific therapies.

Physical

Exercise

Posture and body mechanics as they relate to working and relaxation should be considered in musculoskeletal pain and neurovascular disorders.7 Poor posture is thought to affect most people, but when there is nociceptive activity in a muscle, further nociceptive input, caused by poor posture, might trigger a greater pain response. It has been proposed that posture related to sitting, standing, and sleeping be discussed with the chronic head and neck pain sufferer. Patients are trained to sleep on their back or side, emphasizing a neutral spine position. Sitting with appropriate lumbar support and taking regular breaks from sitting hunched over a workstation are recommended. Good head position requires keeping the ear aligned over the shoulder and hip while sitting and standing. Appropriately modifying the workstation and ensuring eyewear is well-adjusted will prevent anterior head position (jutting the head forward) and eyestrain. Jaw position is also significantly affected by anterior head positioning.8 Patients should also be informed to keep the tongue touching the palate with their teeth unclenched. In certain situations, if cervical spine range of motion needs correction, physical therapy involving cervical mobilization techniques may be used. These techniques, whether direct (manual) or indirect (through specific therapeutic exercises), address dysfunctions found in the cervical spine.9 Treatment is aimed at restoring normal joint relationships and range of motion as well as restoring muscles to their original resting length. Traction, moist heat, ultrasound, and massage are used only as needed to facilitate the mobilization.

Trigger-Point Therapy

Trigger-point injections serve as a diagnostic and therapeutic technique. In myofascial pain, injecting local anesthetic (usually 1 percent procaine) into the tender or active trigger point will decrease the pain temporarily.7,8 It is believed this should be done to relieve the pain so that the patient may function normally for some time, thereby allowing central inhibition to activate. Doing the trigger point injections without addressing perpetuating factors and providing an exercise program has limited value.10

There are other means whereby the trigger point may be converted from active to latent, using spray and stretch, massage, moist heat, ultrasound, electrical stimulation, or other distraction techniques.8,10-12 Applying a distraction stimulus (cold in fluoromethane spray and stretch) allows the muscle to be exercised without restriction. This normal function may be the necessary input to trigger central nervous system inhibition. Botulinum toxin has been described for muscle pain and headache.13 Its function is likely independent of the muscle paralysis it creates, instead it may exert its effect by reducing peripheral neural sensitization.14 Acupuncture points often coincide with the trigger points, and needling these points may in part affect pain through peripheral and central processes. Acupuncture may not be more effective than placebo or massage.15,16

Nerve block

Neural blockade is useful in neuropathic pain conditions. Neuropathic pain by definition requires there to be damage to the peripheral or central nervous system to activate the pain mechanisms.17 The injury may be obvious, such as that following nerve severance or stroke, or minor, such as that as following bruising, infection, or compression. Broadly neuropathic pain is defined as sympathetically maintained and sympathetically independent pain.18 Neural blockade is effective in differentiating sympathetically maintained pain (complex regional pain syndrome) from sympathetically independent pain. It may also be effective in controlling sympathetically maintained pain if used repetitively. Stellate ganglion blocks, phentolamine infusion,19 and sphenopalatine blocks have been described as useful in obtaining a chemical sympathetic block. Somatic block may help identify the pain source. Rarely is this effective as an isolated therapy. Steroid combinations may provide prolonged relief, but care should be exercised because local submucosal steroid use may result in tissue sloughing or if the steroid is injected into the face, the resultant fat necrosis may produce dimpling. Lidocaine infusion (200 mg over one hour) may be used therapeutically in various forms of neuropathic pain.20 It is suggested that response to intravenous lidocaine may predict who responds to the lidocaine analogue mexiletine.

Spinal blocks, including selective nerve root block and epidural and facet injections are useful if there is a local nociceptive source driving the pain. Often magnetic resonance or other imaging points to the nociceptive source. This may then be addressed using fluoroscopic guided procedures. Placing a steroid at the source may help reduce the inflammatory driver and allow physical therapy and exercises to restore function.

Neural blockade with medications other than local anesthetics and steroids has been described for facial pain. Neural destruction may be intentionally created with alcohol or glycerol. Creating anesthesia dolorosa or deafferentation pain should be considered prior. Studies with streptomycin applied to patients with trigeminal neuralgia have not been effective in placebo-controlled trials.

Topical Therapy

The use of topical therapies has not been well-studied. There is some evidence that capsaicin applied regularly will result in desensitization and relief in neuropathic pain. This may deplete substance P and thereby desensitize the pain site. The recommended dose is five times per day for five days and then three times per day for three weeks. If the patient cannot withstand the burning produced by the application, the addition of topical local anesthetic, such as 4 percent lidocaine gel, may prove useful. Topical anesthetics on their own are effective in acute pain states and have limited use in chronic pain. Lidocaine patches are beneficial if the pain is extraoral, but continuous intraoral delivery is a challenge. Using a neurosensory shield may allow longer applications intraorally.21 The dentist may manufacture a custom acrylic stent to fit over the pain site. This is held in place, and the topical agent is repeatedly applied to the gingival surface. Clonidine can be applied to the hyperalgesic region by placing the proprietary subcutaneous delivery patch where it is most tender. Alternatively, the use of a 4 percent gel can be compounded and delivered over a larger area. Topical clonazepam (0.5 to 1.0 mg three times per day) has been effective at reducing a burning oral pain.22 Patients were instructed to suck a tablet for three minutes (and then spit it out) three times per day for at least 10 days. Serum concentrations were minimal (3.3 ng/ml) one and three hours after application. Woda hypothesized there was a peripheral not central action at disrupting the neuropathologic mechanism. One may consider using other topical agents such as ketamine, carbamazepine, amitriptyline, nonsteroidal anti-inflammatories, and steroids; but their benefits have not been systematically studied.

Splint -- Intraoral Orthotic Device

There are numerous splint designs and as many theories as to how and why they work for pain. The exact mechanism whereby patients are helped by splints is elusive. It is recommended that the stabilization appliance be used because the relative risk is minimal.23 Splint therapy still remains the indicated therapy for temporomandibular disorders and muscle pain. Its use for migraines, where there is no temporomandibular or muscle involvement, is not well-studied.24 It does not seem that occlusion is a major factor in TMD, and significant alterations in occlusion as a first line of therapy should be avoided.

Surgery

Although not suggested as a therapeutic modality for trigeminal neuropathic pain, surgery is an excellent alternative for trigeminal neuralgia. The most effective surgical approach remains microvascular decompression.25 Advances in microvascular decompression include the use of an endoscope. This allows clearer observation and is less traumatic.26 Gamma knife radiosurgery is a recent advance for trigeminal neuralgia.27 This technique offers a relatively non-invasive means for lesioning the trigeminal nerve adjacent to the pons using a 4 mm collimator helmet. Complications are rare, and to date the author has seen one case of trigeminal dysesthesia attributed to the procedure. There are numerous other surgeries that may be useful in orofacial pain. Use of surgery for TMD depends upon the etiology. Arthrotomy and open joint surgery are far less necessary since the improved use of arthrocentesis and arthroscopy.28 Future surgical care may include neural stimulation. Currently this is experimental.

Pharmacologic

Pharmacologic intervention for chronic orofacial pain is sometimes essential to allow central nervous system inhibition and facilitate the peripheral therapies. It is essential that the dentist treating chronic pain understands that the medications used to alter pain in the trigeminal nerve distribution may act centrally or directly on the nerve to reduce the pain and suffering. Often, the medications fall into categories such at antihypertensives (beta blockers, calcium channel blockers, alpha adrenergic agents), antidepressants (tricyclic antidepressants, selective serotonin reuptake inhibitors, monoamine oxidase inhibitors), antiepileptic drugs (membrane stabilizers, GABAergic drugs), or specific receptor agonists that are not Food and Drug Administration-approved for pain but are commonly used “off label.” Certainly, the classes specifically approved for pain conditions such as anti-inflammatories, muscle relaxants, narcotic and non-narcotic analgesics, triptans, and ergots are also commonly used for the chronic orofacial pain patient.

For chronic benign pain, the goal should be to limit narcotic use. In certain circumstances, there are no alternatives; and carefully controlled use is necessary. It is recommended that patients understand the therapeutic goal is to keep them functional. If they maintain the agreed behavioral function, continued narcotic use should be provided. If these behaviors are not met, withdrawal from this treatment may be needed. It may be useful to have this withdrawal performed by a detoxification specialist. If medication is to be withdrawn, a protocol for this must be outlined. At times, a blinded process is used to help reduce anxiety over stopping the narcotic. Consent is obtained when using the blinded pain cocktail. The medication is reduced usually by 20 percent per week. Care should be provided to deal with withdrawal symptoms.

Table 1 summarizes the common medication classes used in orofacial pain. This is not an exhaustive list, and dentists treating orofacial pain may use other groups not listed.

Behavioral

Following a behavioral evaluation, management is directed at the factors that may affect treatment and determining the most appropriate interventions. Consideration should be given to the following factors:

* Behavioral or operant;

* Emotional;

* Characterlogical;

* Cognitive;

* Side effects;

* Medication use; and

* Compliance.

To reduce behavioral stressors, stress management and relaxation skills are used. Cognitive behavioral training provides skills for coping with daily life stresses, depression, and pain.29,30 In addition, patients are presented with information regarding myofascial pain and operant aspects of pain and medication use.

Conclusion

Because pain comprises nociception, behavior, and suffering, careful attention to creating a comprehensive therapy is essential. The clinician should not revert to a psychogenic etiology as a default, rather, understanding that all pain, no matter what the etiology, has a behavioral component will allow the patient the opportunity to receive behavioral therapy alongside antinociceptive modalities. The current understanding that pain may be generated from peripheral and central mechanisms further warrants the therapy to be aimed not only at the peripheral source, but also at the brain pain inhibition systems. A patient who has a toothache after an extraction or root canal therapy may not have a peripheral source for the pain, rather the pain may be generated by an ongoing process in the trigeminal nucleus or elsewhere in the brain. Treatment aimed solely at the tooth site may only worsen the situation, whereas treatment aimed at stabilizing neural excitability or enhancing central inhibition (e.g., medication and/or behavioral intervention) may reduce the pain, behavior changes, and suffering.

Current advances in knowledge regarding pain mechanisms have made therapy for chronic pain patients more successful. Patients should be afforded therapy from as broad and all-encompassing a base as possible.

References

1. Graff Radford SB, Solberg WK, Atypical odontalgia. J Cal Dent Assoc 14(12):27 32, 1986.

2. Fricton JR, Critical Commentary. A unified concept of idiopathic orofacial pain: Clinical Features. J Orofacial Pain 13(3):185-9, 1999.

3. Mersky H, ed, Classification of chronic pain: description of chronic pain syndromes and definition of terms. Pain, suppl. 3:S1, 1986.

4. Headache Classification Committee of the International Headache Society, Classification and diagnostic criteria for headache disorders, cranial neuralgias, and facial pain. Cephalalgia 8:1-96, 1998.

5. Graff-Radford SB, Disorders of the mouth and teeth. In, Silberstein SD, Lipton RB, Dalessio DJ, eds, Wolff’s Headache and Other Head Pain, 7th ed. Oxford Press, Chicago, Vol 7 2001, pp 475-93.

6. Graff-Radford SB, Treatment contracting for chronic pain patients. Los Angeles Psychologist 13(1):9, 26, 1999.

7. Graff-Radford SB, Regional myofascial pain syndromes and headache, principals of diagnosis and management. Current Pain Headache Reports 5:376-81, 2001

8. Travell JG. and Simons DG, Myofascial Pain and Dysfunction: The Trigger Point Manual. Williams and Wilkins Co, Baltimore, 1988.

9. Maitland GD, Vertebral Manipulation, 4th ed. Butterworths, London, 1977.

10. Graff Radford SB, Reeves JL, Jaeger B, Management of headache: the effectiveness of altering factors perpetuating myofascial pain. Headache 27:186 90, 1987.

11. Mennell JM, Spray-stretch for relief of pain from muscle spasm and myofascial trigger points. J Am Pod Assoc 66:873-6, 1976.

12. Jaeger B, Myofascial referred pain patterns: the role of trigger points. J Cal Dent Assoc 13(3):27-32, 1985.

13. Freund B, Schwartz M, Symington JM, The use of botulinum toxin in temporomandibular disorders: preliminary findings. J Oral Maxillofac Surg 57:916-20, 1999.

14. Royal MA, The use of botulinum toxins in the management of pain and headache. Pain Practice 1:215-35, 2001.

15. Tavola T, Gala C, et al, Traditional Chinese acupuncture in tension type headache a controlled study. Pain 48:325-9, 1992.

16. Ahonen E, Mahlmaki S, et al, Effectiveness of acupuncture and physiotherapy on myogenic headache. A comparative study. Acupunct Electrother Res 9:141-50, 1984.

17. Campbell JN, Raja SN, Meyer RA, Painful sequellae of nerve injury. In, Dubner R, Gebhart GF, Bond MR, eds, Pain Research and Clinical Management. Elsevier, Amsterdam, the Netherlands, 1998.

18. Graff-Radford SB, Facial pain. Curr Opinion Neurolog 13:291-6, 2000.

19. Scrivani SJ, Chaudry A, et al, Chronic neurogenic facial pain: Lack of response to intravenous phentolamine. J Orofacial Pain 13:89-96, 1999.

20. Sinnott CJ, Garfield JM, Strichartz GR, Differential efficacy of intravenous lidocaine in alleviating ipsilateral versus contralateral neuropathic pain in the rat. Pain 80:521-31, 1999.

21. Graff-Radford SB, Facial pain of undetermined origin. In, Rappaport A, Sheftell F, Purdy A, eds, Advanced Therapy of Headache: Case Based Strategies for Management. BC Decker Publishers, Hamilton, Ontario, 1999, pp 263-9.

22. Woda A, Navez M-L, et al, A possible therapeutic solution for stomatodynia (burning mouth syndrome). J Orofacial Pain 12:272-8, 1998.

23. Solberg WK, Temporomandibular disorders: Masticatory myalgia and its management. Br Dent J 160:379-85, 1986.

24. Graff-Radford SB, Forssell H, Oromandibular Treatment. In, Olesen J, Tfelt-Hansen P, Welch KMA, eds, Headaches. Raven Press, New York, 2000 pp 657-60.

25. Janetta PJ, Trigeminal neuralgia: treatment by microvascular decompression. In, Wilkins RH, Ragachary SS, eds, Neurosurgery. McGraw Hill, New York, 1996, pp 3961-8.

26. Jarrahy R, Berci G, Shahinian HK, Endoscope-assisted microvascular decompression of the trigeminal nerve. Otolaryngol Head Neck Surg 123(3):218-23, 2000.

27. Young RF, Vermeulen SS, et al, Gamma knife radiosurgery for treatment of trigeminal neuralgia. Idiopathic and tumor related. Neurology 48:608-14, 1997.

28. Montgomery MT, Van Sickels JE, et al, Arthroscopic TMJ surgery: Effects on signs, symptoms, and disc position. J Oral Maxillofac Surg 47:1263-71, 1989.

29. Reeves JL, EMG-biofeedback reduction of tension headaches: a cognitive skills training approach. Biofeedback Self Regulation 1:217-25, 1976.

30. Holroyd KA, Andresik F, Westbrook T, Cognitive control of tension headaches: a cognitive skills training approach. Cognitive Therapy and Research 1:121-33, 1977.

To request a printed copy of this article, please contact/Steven B. Graff-Radford, DDS, 444 S. San Vicente, #1101, Los Angeles, CA 90048 or at graffs@cshs.org.

Table 1. Medications Used in Orofacial Pain

Analgesics

Narcotic

Non-narcotic

Antidepressants

Tricyclic antidepressants

Selective serotonin reuptake inhibitors

Monoamine oxidase inhibitors

Antiepileptic drugs

Membrane stabilizers

GABAergic agents

Antihypertensives

Alpha blockers

Beta blockers

Calcium channel blockers

Muscle relaxants

Serotonin antagonists

Serotonin agonists

Ergots (nonselective)

Triptans