Interdisciplinary Orofacial Pain Management

John Johnson DDS, MS and Peter Bertrand DDS

As evidenced by the topics presented in this clinical guide, orofacial pain disorders comprise a wide range of conditions, thus when evaluating an orofacial pain patient, the clinician may face a formidable diagnostic challenge. The differential diagnoses for an orofacial pain complaint may include conditions from a variety of categories: musculoskeletal, inflammatory, infectious, neurovascular, neoplastic, metabolic, endocrine, autoimmune and neuropathic disorders.1 Such conditions may produce acute or chronic symptoms, and present as single or co-existing disorders that may share complicated inter-relationships.

When history and examination do not indicate a clearly identifiable etiology for a patient’s pain (i.e. trauma, infection, neoplasm, etc.), the provider should approach the patient with an interdisciplinary mindset. Interdisciplinary management does not necessarily mandate that a patient must be assessed and treated by multiple professionals. An individual provider who possesses a broad array of skills may be in the best position to deliver optimum interdisciplinary orofacial pain management. Such skills are based upon an expanded understanding of orofacial pain that appreciates the unique anatomic and physiologic complexities of cranial nerve systems and incorporates recent advances in the neurobiology of pain. Contemporary neuroscience validates the need for an interdisciplinary approach towards orofacial pain practice. It moves the provider beyond a simple biomechanical or inflammatory concept of pain, substantiates the biologic basis for the biopsychosocial model of pain, and provides pathophysiologic links between orofacial pain disorders and common comorbid pain conditions such as irritable bowel or fibromyalgia.

Neurobiologic Considerations

One of the difficulties in dealing with orofacial pain complaints relates to the structural complexity of the trigeminal nerve system. It is incumbent for clinicians to distinguish true sources of pain from trigeminal sites of pain and to discern the locations of all non-trigeminal sources of pain. The trigeminal sensory nuclei receive extensive input from structures within the brain stem and midbrain that process sensory information from tissues outside the face. The trigeminal interpolaris and spinal tract nuclei receive convergent sensory input from the facial, glossopharyngeal and vagus nerves, as well as the upper cervical nerves (C1-4).2 Convergent nociceptive input from non-trigeminal afferent neurons provides an anatomic explanation as to how disorders in remote regions of the head and neck may refer pain to the face.

Another important consideration in orofacial pain is the capability of non-trigeminal brain centers to induce non-volitional trigeminal motor responses, muscle activity that has been often labeled as “parafunction”. Integrative centers within the brain stem, such as the parvocellular reticular formation and paratrigeminal nucleus, receive both noxious and non-noxious visceral, cutaneous and autonomic input, and via connections with the trigeminal nuclear complex, may produce a masticatory muscle response.3 Similarly activity in higher brain centers, such as the limbic system and prefrontal cortex, can engage descending neural circuits also capable of inciting masticatory muscle activity.4 Concurrent with induced masticatory responses, hypoglossal, spinal accessory, facial, glossopharyngeal and vagal motor centers may also be activated. Afferent input from tissues controlled by these nerves may contribute to the wide constellation of symptoms seen in orofacial pain patients.

Persistent, non-functional masticatory muscle activity may have significant biologic and clinical consequences. Even low levels of muscle activity excite metaboreceptors that send impulses to the central nervous system via group III and IV afferents (A-delta and C fibers) 5, the same classes of first order neurons activated by peripheral nociceptors. Metaboreceptor activity of sufficient intensity and duration may be noxious and produce pain. Excessive metaboreceptor activity may lead to central sensitization, facilitate the referred pain phenomenon associated with myofascial pain, and induce masticatory muscle co-contraction. Persistent masticatory muscle activation may also contribute to pathologic changes within the temporomandibular joint (TMJ). Prolonged periods of increased intra-articular pressure have been associated with local tissue hypoxia, free radical formation and oxygen reperfusion injury, all factors thought to play a role in the genesis of TMJ osteoarthritis and disc displacements.6,7 Interestingly, the presence of muscle pain may also decrease proprioceptive feedback, thus a patient may not be fully aware of the extent of their muscle parafunction or overuse.8

There is an increasing body of evidence that many orofacial pain patients frequently possess other remarkable physical and mental health concerns. Turp and colleagues found that 82% of facial pain patients also had additional pain complaints outside the distribution of the trigeminal system.9 Based on an anonymous self-report survey, 68% of patients referred to a university orofacial pain center indicated a history of physical or sexual abuse.10 Recent investigations have shown that patients with temporomandibular disorders often have co-existing conditions including irritable bowel disease, fibromyalgia, migraine, panic disorder and others.11 The link between these seemingly disparate disorders is the potential of a shared neuropathophysiology involving alterations in hypothalamic-pituitary-adrenal axis, autonomic nervous system and limbic system-prefrontal cortex responses.12 Hyperactivity, hypoactivity or lack of coordination within or between the aforementioned systems could lead to dysfunctional allostasis, changes in vasomotor responses, modifications in respiration and alterations in sensory processing.

Assessment and Treatment

Interdisciplinary orofacial pain management begins with a comprehensive patient history. The most expeditious way to obtain such a history is via a detailed patient questionnaire. Such an instrument seeks not just information about the chief complaint, but also records a complete medical and treatment history, asks about any site of pain anywhere in the body, assesses affect, checks for awareness of muscle parafunction, reviews personal habits, seeks insight into vocational and family concerns, inquires about negative life events (i.e. abuse, assault, childhood neglect, etc.), and solicits information about sleep. A detailed history, a complete oral, head and neck examination that distinguishes sites from sources of pain, and appropriate imaging and/or laboratory studies are foundational for establishing a list of differential diagnoses and contributing factors.13 In some cases, the provider may have the training, experience and resources to handle all of the patient’s treatment needs and address the relevant contributory factors. In other instances, the assistance of additional practitioners may be required. Healthcare providers often involved with the global management of orofacial pain patients include: dentists, oral surgeons, primary care physicians, neurologists, physiatrists, physical therapists, psychiatrists, psychologists, and rheumatologists.

A physiologically based, interdisciplinary treatment algorithm for orofacial pain disorders may be summarized by following:

  1. Consider the impact of all sources of pain, including those outside the orofacial region. Non-trigeminal sources of nociception may refer pain cephalad, facilitate cranial nerve mediated muscle parafunction, induce co-contraction, and disrupt sleep.
  2. Reduce masticatory and cervical muscle overuse to decrease fatigue, pain and joint overloading. Employ behavioral strategies that increase parafunctional awareness and diminish the brain activity that may facilitate inappropriate muscle use.14
  3. Reduce physiologic arousal. Use relaxation techniques, such as diaphragmatic breathing and imagery, to affect brain regions that may adversely influence pain thresholds, muscle activity or sleep. Recognize the need to address negative affect, stressful personal-family-vocational issues and the excessive use of stimulants (caffeine, nicotine, etc.).
  4. Enhance sleep. Explore all factors that can delay, disrupt or lighten sleep. Educate patients about the importance of sleep hygiene measures and cognitive behavioral strategies such as sleep restriction, stimulus control and relaxation techniques.15 When prescribing sedative-hypnotic medications, give preference to those that promote stage 3 and stage 4 sleep.

References

  1. Diagnostic Classification of Orofacial Pain Disorders, in Orofacial Pain, Guidelines for Assessment, Diagnosis and Management, Okeson J.P. (Ed). Quintessence Books: Chicago. 1996, p 45-52.
  2. Sessle BJ. Acute and chronic craniofacial pain: brainstem mechanisms of nociceptive transmission and neuroplasticity, and their clinical correlates. Crit Rev Oral Biol Med. 2000;11(1):57-91.
  3. Ter Horst GJ, Copray JC, Liem RS, Van Willigen JD. Projections from the rostral parvocellular reticular formation to pontine and medullary nuclei in the rat: involvement in autonomic regulation and orofacial motor control. Neuroscience. 1991;40(3):735-758.
  4. Nieuwenhuys R. The greater limbic system, the emotional motor system and the brain. Prog Brain Res. 1996;107:551-580.
  5. Adreani CM, Hill JM, Kaufman MP. Responses of group III and IV muscle afferents to dynamic exercise. J Appl Physiol. 1997;82(6):1811-1817.
  6. Milam SB, Schmitz JP. Molecular biology of temporomandibular joint disorders: proposed mechanisms of disease. J Oral Maxillofac Surg. 1995;53:1448-1454.
  7. Nitzan DW. The process of lubrication impairment and its involvement in temporomandibular joint disc displacement: a theoretical concept. J Oral Maxillofac Surg. 2001;59:36-45.
  8. Rossi S, della Volpe R, Giananneschi F, Ulivelli M, Bartalini S, Spidalieri R, Rossi A. Early somatosensory processing during tonic muscle pain in humans: relation to loss of proprioception and motor ‘defensive’ strategies. Clin Neurophysiol. 2003;114:1351-1358.
  9. Turp JC, Kowalski CJ, O’Leary, Stohler CS. Pain maps from facial pain patients indicate a broad pain geography. J Dent Res. 1998;77(6):1465-1472.
  10. Curran SL, Sherman JJ, Cunningham LL, Okeson JP, Reid KI, Carlson CR. Physical and sexual abuse among orofacial pain patients: linkages with pain and psychological distress. J Orofac Pain. 1995;9(4):340-346.
  11. Aaron LA, Burke MM, Buchwald D. Overlapping conditions among patients with chronic fatigue syndrome, fibromyalgia and temporomandibular disorder. Arch Intern Med. 2000;160:221-227.
  12. Mayer EA. The neurobiology of stress and gastrointestinal disease. Gut. 2000;47:861-869.
  13. Diagnostic Classification of Orofacial Pain Disorders, in Orofacial Pain, Guidelines for Assessment, Diagnosis and Management, Okeson J.P. (Ed). Quintessence Books: Chicago. 1996, p 19-44.
  14. Carlson CR, Bertrand PM, Ehrlich AD, Maxwell AW, Burton RG. Physical self-regulation training for the management of temporomandibular disorders. J Orofac Pain. 2001;15(1);47-55.
  15. Jacobs GD, Pace-Schott EF, Stickgold R, Otto MW. Cognitive behavior therapy and pharmacotherapy for insomnia. Arch Intern Med. 2004;164:1888-1896.