OBJECTIVE: To report on a patient with trigeminal neuralgia who responded positively to combined carbamazepine/oxycodone treatment. CASE SUMMARY: A 48-year-old woman with a 4-month history of left facial pain consisting of episodes lasting less than 5 minutes was brought to our institution for clinical evaluation. Clinical, laboratory, and neuroradiologic findings led to a diagnosis of idiopathic trigeminal neuralgia. Carbamazepine treatment was started at 200 mg every 12 hours and increased at discharge to 300 mg every 8 hours. Two weeks later the patient was readmitted with trigeminal neuralgia symptoms that had persisted since the previous admission, although they had decreased in intensity. Carbamazepine was reduced to 200 mg every 8 hours and oxycodone 5 mg every 12 hours was added to the treatment regimen, with a complete resolution of pain within 7 days. DISCUSSION: Pathophysiological mechanisms involved in both the genesis and the maintenance of trigeminal neuralgia have not yet been defined. Several hypotheses could explain this disorder, ranging from peripheral neural ectopic pacemaker to central disinhibition. Both the interruption of the sodium channel and the modulation of both κ- and μ-opioid receptors contributed to antinociceptive effects in trigeminal neuralgia. CONCLUSIONS: Treatment with a combination of carbamazepine, a sodium channel blocker, and oxycodone, a mixed κ- and μ-opioid receptor agonist, may be useful in alleviating symptoms of trigeminal neuralgia.
OBJECTIVE: To report on a patient with trigeminal neuralgia who responded positively to combined carbamazepine/oxycodone treatment. CASE SUMMARY: A 48-year-old woman with a 4-month history of left facial pain consisting of episodes lasting less than 5 minutes was brought to our institution for clinical evaluation. Clinical, laboratory, and neuroradiologic findings led to a diagnosis of idiopathic trigeminal neuralgia. Carbamazepine treatment was started at 200 mg every 12 hours and increased at discharge to 300 mg every 8 hours. Two weeks later the patient was readmitted with trigeminal neuralgia symptoms that had persisted since the previous admission, although they had decreased in intensity. Carbamazepine was reduced to 200 mg every 8 hours and oxycodone 5 mg every 12 hours was added to the treatment regimen, with a complete resolution of pain within 7 days. DISCUSSION: Pathophysiological mechanisms involved in both the genesis and the maintenance of trigeminal neuralgia have not yet been defined. Several hypotheses could explain this disorder, ranging from peripheral neural ectopic pacemaker to central disinhibition. Both the interruption of the sodium channel and the modulation of both κ- and μ-opioid receptors contributed to antinociceptive effects in trigeminal neuralgia. CONCLUSIONS: Treatment with a combination of carbamazepine, a sodium channel blocker, and oxycodone, a mixed κ- and μ-opioid receptor agonist, may be useful in alleviating symptoms of trigeminal neuralgia.