Mitchell B. Max
Pain caused by a lesion of the peripheral or central nervous system (CNS) is commonly termed neuropathic pain. This chapter will consider only lesions of peripheral nerves.
Neurogenic pain in the orofacial region, as in other areas, can result from nerve trauma, deafferentation, or amputation (eg, vascular compression, neoplasia, bone fracture, root canal therapy, maxillofacial surgery); infection (eg, postherpetic neuralgia, HIV-related neuropathies); or metabolic disturbance (eg, diabetic neuralgia). However, the latter is not frequently associated with orofacial pain.
Orofacial Neuropathic Pain Conditions
Some patients develop posttraumatic neuropathic pain following trauma to the face, root canal treatments, tooth extractions, or even minor procedures. The pain is of moderate to severe intensity, often burning, and usually continuous. Typically, it is unilateral; the pain may spread across dermatomes but rarely crosses the midline. A related condition, atypical odontalgia, is a severe throbbing pain in the tooth without any evident major pathology. The pain is commonly continuous and burning but can also be pulsatile, episodic, and migrating. Many authors report trauma or previous dental treatment, such as tooth extraction or root canal therapy, as the initiating event for atypical odontalgia and consider this condition to be “phantom toothache.” It may be misdiagnosed as dental pain, leading to unnecessary dental and surgical treatment (see also chapter 20). Repeated interventions to relieve atypical odontalgia may induce posttraumatic neuropathic pain and be a significant factor in increasing comorbidity.
Two subsets of trigeminal neuralgia are recognized: idiopathic (classic) and neuralgia secondary to other pathologies such as multiple sclerosis and CNS tumors. The pain is severe and unilateral; it is usually described as sharp, shooting, stabbing, or electric in nature and is sometimes accompanied by background pain. The pain can be spontaneous or triggered by minor stimulation of specific trigger zones.
Postherpetic neuralgia is a painful condition that follows acute herpes zoster reactivation and can remain for months or even years after the rash and blisters have healed. It occurs most often in older people and in patients who are immuno-suppressed. The pain is described as severe, sharp, throbbing, or stabbing and may be accompanied by skin allodynia.
Readers should consult Orofacial Pain: Guidelines for Assessment, Diagnosis, and Management1 from the American Academy of Orofacial Pain for further information.
Apart from idiopathic trigeminal neuralgia, a unique condition with its own treatment approach (discussed in a later section), it will be assumed that drug responses in neuropathic pain are similar no matter where in the body the pain originates. This assumption is necessary because only randomized clinical trials (RCTs) provide reliable evidence about analgesic responses, and too few RCTs have been conducted in orofacial pain to consider it separately. Recent reviews have proposed useful algorithms for the treatment of neuropathic pain.2,3
As described in previous chapters, therapeutic strategies should include a discussion of neuropathic pain causes and prognosis, as well as behavioral advice to the patient. Psychologic support is often indicated, as is information about the use and abuse of alternative therapies. While the drug management described in this chapter is supported by scientific evidence, the use of these medications is not without risk of side effects and medical complications. It is strongly recommended that clinicians prescribe these drugs with the collaboration of a family physician, neurologist, or oral medicine specialist.
Prevention of Neuropathic Pain
Preemptive analgesia induced by anesthetic blocks during surgery can prevent pain related to primary afferent hyperactivity and central sensitization (see chapters 5 and 7). Early antiviral treatment for acute herpes zoster, particularly in elderly patients, can decrease the incidence of postherpetic neuralgia.
Treatment for Neuropathic Pain (Excluding Trigeminal Neuralgia)
The drugs most commonly used for treating neuropathic pain are shown in Table 24-1. These drugs are grouped into sections according to the strength of evidence for effectiveness and toxicity. The first section describes the opioids, antidepressants, and anticonvulsants, which are roughly equipotent, and a topical lidocaine patch, which is partly effective in postherpetic neuralgia.
|Table 24-1 Drugs commonly used to treat neuropathic pain|
|Strong evidence for benefit
|μ-Receptor opioid agonists: morphine, oxycodone, fentanyl, etc||Variable||Sedation, nausea||Strong evidence for efficacy in PHN|
|Tramadol||50–100 mg tid or qid||Sedation, nausea, rare seizures||Less constipation|
|Tricyclic antidepressants: amitriptyline, nortriptyline, desipramine, imipramine||Start at 10–25 mg/day; titrate to 75–125 mg/day||Orthostatic hypotension, anticholinergic effects, risk of malignant arrhythmia or heart block in ischemic heart disease||Nortriptyline may be as effective as amitriptyline, and sedation, hypotension, anticholinergic side effects are less common|
|duloxetine, paroxetine, citalopram||40–60 mg/day (duloxetine)||Anticholinergic effects, dry mouth, constipation, increased sweating; paroxetine may raise tricyclic antidepressant concentrations threefold to sevenfold||Duloxetine is FDA cleared in the USA for the treatment of painful diabetic neuropathy|
|Gabapentin||1,800–3,600 mg/day||Sedation, ataxia||Efficacy similar to tricyclic antidepressants in diabetic neuropathy and PHN, but has no risk of hypotension or arrhythmia|
|Pregabalin||Start at 50 mg tid; titrate up to 300 mg/day||Dizziness, sedation||Good results in the treatment of PHN and diabetic neuropathy|
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