In addition, diagnostic and treatment errors are common, which can increase pain and problems. He pointed to one study of 64 patients that found prior to a diagnosis of atypical odontalgia, they collectively visited 16 different specialists, from a dentist to an oncologist to a psychiatrist. In fact, “frustrated clinicians may refer patients to a psychiatrist if no apparent cause for pain can be identified.” Dr. Foreman said statistics show psychiatric morbidity often results from persistent pain; however, “it is seldom the cause. One common dental example is “burning mouth syndrome,” which is often labeled psychogenic. Yet, evidence now shows a neurological etiology is more likely, he said.
A thorough history is essential in diagnosing and managing atypical odontalgia. Patients should be asked about the duration of pain and its cause (eg, caries, injury) and the nature of the pain. For example, deep, dull, aching, intermittent pain of variable intensity suggests myofascial pain, which is often due to muscle overuse, such as bruxism and work habits. Relief is often achieved after the cause is controlled. Conversely, sharp, burning, tingling, or stabbing pain that is constant or intermittent suggests neuropathic pain. Relief is often difficult to achieve and may follow deafferentation, such as extractions, surgery, endodontia, or implants.
“Dental neuropathies are difficult to diagnose and treat,” he said. The “smoking gun” in the process of complex events that lead to the development of central sensitization—and, eventually, atypical odontalgia—may well be prolonged C-fiber activity, he said, because approximately 87% of dental pulp fibers are type C.
Since atypical odontalgia is a central sensitization disorder,invasive procedures that could further exacerbate the situation “should be avoided.” Once central sensitization has developed, pain is likely to continue despite treatment, Dr. Foreman said, adding, “this is a trap for the unwary dentist.” Instead, clinicians should place their emphasis on management.
Preemptive analgesia may be used to try to prevent atypical odontalgia. For example, effective long-acting local anesthesia, supported centrally with perioperative NSAIDs, can help block events that lead to onset of central sensitization as well as development of postoperative rebound pain, reducing analgesic needs. General anesthesia alone will not block C-fiber activity, he pointed out.
Postsurgery, “pain medications should be time contingent, not pain contingent,” he said. “This maintains optimal drug levels and helps prevent breakthrough pain.” Tricyclics such as amitriptyline and nortriptyline are useful. He recommended starting with a low dose (10 mg), increasing gradually for the best effect with minimal side effects. Patients should be warned that such agents are not a cure but can help reduce discomfort. Acetaminophen has a mild effect on central pain if used as an adjunct; however, high dosages should be avoided.
Anti-neuropathic drugs such as clonazepam, gabapentin and pregabalin may provide relief, Dr. Foreman said; however, carbamazepine is seldom prescribed due to significant side effects. Ketamine acts on the NMDA receptor site but also has “major side effects.”
What’s important to understand, he said, is that for orofacial pain of nondental origin, “the site of the pain is not always its source. Where the diagnosis is in doubt and the patient is insistent, proceed with caution.”