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Chronic Pain Syndromes: How to Break the Cycle, Part 2

Chronic Pain Syndromes: How to Break the Cycle, Part 2

Establishing the cause of chronic pain is crucial because treatment based on the mechanism of the pain is most likely to be successful. In part 1 of this 2-part article (CONSULTANT, April 1, 2008), we discussed the management of pain associated with knee osteoarthritis. Here we focus on the diagnosis and treatment of trigeminal neuralgia and radicular low back pain.

Trigeminal neuralgia presents with sudden, primarily unilateral, brief, stabbing, recurrent pain in the distribution of 1 or more branches of the fifth cranial nerve.1 Although trigeminal neuralgia is the most common cranial nerve neuralgia, the yearly incidence is only about 4 per 100,000, increasing to 20 per 100,000 after the age of 60 years.2 Women are more often affected than men.

Pathophysiology. Trigeminal neuralgia can be classified as primary (idiopathic) or secondary (symptomatic). Underlying processes associated with the secondary form include demyelinating disease, such as multiple sclerosis (often bilateral) or a posterior fossa tumor (eg, meningioma). Studies have suggested that about 10% of patients with trigeminal neuralgia may have a causative intracranial lesion.3

Although there are multiple theories, the exact pathophysiology of trigeminal neuralgia is unknown. One of the current theories supported by ultrastructural analysis is the ignition hypothesis. According to this theory, sensory axons of cranial nerve V become demyelinated in the primary form because of sustained or pulsatile microvascular compression of the trigeminal nerve or ganglia. In the secondary form, demyelination occurs because of compression from a tumor or multiple sclerosis lesion. Once structural damage has occurred to cranial nerve V or its ganglia, ectopic impulse discharges, spontaneous and triggered after discharges, and crossed excitation among neighboring afferent fibers can all lead to pain paroxysms. This could explain why these patients have trigger areas, since electrical activity from A-beta fibers (which respond to light touch) activates nociceptive fibers (C and A-delta fibers).4

Diagnosis. In the idiopathic and secondary forms, the attacks are periodic and of short duration, often with lucid intervals. The patient typically describes sharp, shooting, unilateral pain usually in the distribution of the maxillary branch of the fifth cranial nerve (V2) or the mandibular branch (V3). The ophthalmic branch (V1) is involved in fewer than 5% of cases. If V1 is involved, other possible diagnoses, including postherpetic neuralgia, should be excluded. The right cranial nerve V is affected more often than the left; the right to left ratio is 1.5 in the primary form and 2.4 in the secondary.5

Patients often describe activities that bring about symptoms, including chewing, toothbrushing, or hair-brushing, and they often have associated tactile trigger areas. If a patient has pain with swallowing, consider glossopharyngeal nerve neuralgia.1

The secondary form of trigeminal neuralgia typically affects younger persons. Any patient younger than 40 years who has trigeminal neuralgia should undergo a workup for an underlying disease process. In most patients who have the primary form, the results of sensory and motor neurological examinations are normal.

Other diagnoses that can be included in the differential for unilateral facial pain and that must be excluded are:

• Dental pain (eg, pulpitis, fractured tooth, temporomandibular joint disorder, phantom tooth pain).
• Temporal arteritis.
• Carotodynia.
• Cluster headache.
• A cavernous sinus lesion (often a metastatic lesion from the breast, lung, or prostate).
• Postherpetic neuralgia.

A misunderstood cause of facial pain is atypical facial pain syndrome (pain of unknown origin). The diagnosis of atypical facial pain should be made only after all other causes have been ruled out. Unlike patients with trigeminal neuralgia, these patients complain of constant, poorly localized pain often without pain-free intervals or trigger areas. Use of the McGill Pain Questionnaire with close attention to descriptor choice can help distinguish atypical facial pain from trigeminal neuralgia.6 If the history and physical examination suggest either primary or secondary trigeminal neuralgia, additional studies are warranted, including an MRI scan with gadolinium and thin cuts (less than 1 mm) through the trigeminal nerve.7 Particular attention should be paid to the cavernous sinus and Meckel cavity, where the gasserian ganglion is located. The MRI scan can help identify or rule out underlying mass lesions, vascular compression of cranial nerve V, and demyelinating lesions. If multiple sclerosis is suspected, a lumbar puncture can be ordered. Neurophysiological diagnostic testing of the trigeminal reflexes can help differentiate primary (normal reflexes) and secondary trigeminal neuralgia with a sensitivity of 96% and a specificity of 93%.5,8

Medical therapy. The first line of treatment for trigeminal neuralgia is medical management. Once the diagnosis has been made and treatment options are being discussed, a resource to which patients can be referred for more information is the Trigeminal Neuralgia Association Web site ( More than 50% of patients with trigeminal neuralgia have periods of remission that can last longer than 6 months.1 Thus, at the start of treatment, it is important to suggest to the patient that the drug dosage can be tapered as soon as 12 weeks after adequate pain control has been achieved.

A baseline blood and metabolic profile is needed before drug therapy is started. (Table 1 lists selected medications for trigeminal neuralgia.) Initially, monotherapy is used. If this is ineffective or if side effects occur, a second agent can be added. Carbamazepine, an anticonvulsant, is one of the most studied medications, and its efficacy has been demonstrated.9 A slow titration is started at 100 mg PO bid. The dose is increased by 50- to 100-mg increments up to a maximum dosage of 1200 mg/d based on efficacy, side-effect profile, and serum levels (4 to 12 µg/mL). Order laboratory studies at 1-month intervals during the initiation of treatment with close attention to the possible development of blood dyscrasias (aplastic anemia, agranulocytosis) and hyponatremia. Other adverse effects associated with carbamazepine include somnolence, gait disturbances, and a rash that can develop into Stevens-Johnson syndrome.

Oxcarbazepine, which is associated with fewer adverse effects, can be used instead of carbamazepine. Start with a dosage of 150 mg PO bid, and increase up to a total daily dose of 600 to 2400 mg/d. The median effective total daily dose of oxcarbazepine for newly diagnosed trigeminal neuralgia is 750 mg (1200 mg for refractory disease). In a small study, lamotrigine was effective in treating refractory trigeminal neuralgia at a maintenance dosage of 400 mg/d.10 Other medications that can be used as a sole agent or in combination with carbamazepine or oxcarbazepine are gabapentin,11 pregabalin,12 tricyclic antidepressants (amitriptyline, nortriptyline), and baclofen.7 Second-generation agents such as pregabalin (dose range, 150 to 600 mg/d) and gabapentin (up to 3600 mg/d) have fewer adverse effects than first-line agents, but they have not been as extensively studied in trigeminal neuralgia. Thus, evidence of their efficacy is based on case reports and extrapolation from other neuropathic pain models.13,14 Opioids are not first-line agents for trigeminal neuralgia, and their use should be restricted to short periods in which rescue medications are needed.



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