Objective: We examined whether ketamine, which is a noncompetitive blocker of N-methyl-D-aspartate (NMDA) receptors, had the ability to relieve glossopharyngeal neuralgia. A tentative hypothesis is that glossopharyngeal neuralgia involves hyperactivity in the central nociceptive neurons and that the development of this hyperactivity is dependent on activation of NMDA receptors.
Clinical presentation: The pain syndrome of this 56-year-old woman had lasted for approximately 7 years and was localized to the posterior pharynx, tonsillar region, and base of the tongue, with radiation to the left deep ear structures. Pain was provoked by swallowing.
Intervention: It was first determined in a double-blind experiment that intravenous ketamine markedly reduced pain. The optimal oral dose (60 mg administered six times/d) was observed in an open dose escalating trial. In an N of 1 trial, the patient received double blindly either oral ketamine (60 mg administered six times/d) or placebo during 10 2-day periods. Ketamine caused marked pain relief, as shown by statistically significant pain relief and reduction of pain intensity. Pain caused by swallowing also was reduced by ketamine. Pain relief was associated with some side effects; however, the treatment was well tolerated by the patient.
Conclusion: This case report shows that ketamine-induced NMDA receptor blockade significantly relieved glossopharyngeal neuralgia in this patient. Therefore, NMDA receptors may play a significant role in the pathogenesis of the pain syndrome described.