Trigeminal neuralgia (TN) represents a debilitating neuropathic pain condition occurring in as many as 20 cases per 100,000 people per year after age 60. 11, 12 Symptoms are characterized by paroxysmal episodes of severe, sharp pain occurring in one or more branches of the trigeminal nerve, frequently following innocuous mechanical stimuli. Although a number of etiologically distinct conditions have been implicated in the development of TN, demyelination at the junction of central and peripheral myelin in the trigeminal nerve likely represents the common pathway for the development of TN. 13 Compression by vascular and neoplastic structures, as well as primary demyelinating disorders, may in this way cause ephaptic transmission, whereby inoccuous signals carried by Ia fibers may be transmitted to nociceptive fibers. Patients with this condition usually obtain an initial robust analgesic response to regular, prophylactic use of carbamazapine. However, this often wanes. Second line medical therapies tend to have less robust analgesic efficacy for reducing the number and frequency of episodic surges of pain intensity (see AAN guidelines for medical management of TN published in Neurology last yr). The significant disability imposed by TN has led to the exploration of myriad treatment modalities for pain relief, including a number of interventional approaches.