Abstract

Classic idiopathic trigeminal neuralgia (TN), with distinctive, severe paroxysms of electric, shock-like pains in a unilateral trigeminal distribution, is a well-defined facial pain syndrome. Pharmacologic and surgical treatments are often effective, at least initially. The patient is usually asymptomatic between paroxysms.1,2 There are patients with persisting trigeminal pain in between otherwise typical paroxysms, generally labeled atypical TN.2 This has been proposed to be the long-term consequence of untreated or undertreated classic TN.3 Treatment of atypical TN is often frustrating as pharmacologic and surgical interventions do not show robust or lasting benefits. Constant pain is particularly refractory. Outcome data from microvascular decompression with classic TN shows excellent or good pain relief in 97% immediately postoperatively and in 80% of those with 5-year follow-up. With atypical TN, only 51% show good or excellent pain relief at 5 years.4 In this issue of Neurology ®, Obermann et al.5 report the results of an electrophysiologic analysis of trigeminal nociceptive pathways in patients with typical TN and those with persisting chronic pain in between paroxysms (i.e., atypical TN). Obermann et al. utilize a novel, concentric stimulating electrode which has previously been shown to preferentially depolarize superficial nociceptive A-delta fibers and relatively …

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