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Intra-arterial Modulation of the Trigeminal Nerve Ganglion in Patients with Refractory Trigeminal Neuralgia.
BACKGROUND AND PURPOSE: Nerves and nerve ganglions are supplied by segmental arteries and the vasa nervorum, but the intra-arterial route has not been used for diagnostic or therapeutic purposes. We present the results of intra-arterial delivery of medication for modulating trigeminal nerve ganglion function in patients with refractory trigeminal neuralgia.
METHODS: We administered intra-arterial lidocaine in doses up to 50 mg in the middle meningeal artery territory adjacent to the arterial branch that supplies the trigeminal nerve ganglion. We performed electrophysiologic monitoring to serially assess the latency and amplitude of R1 and R2 responses in the blink reflex before and concurrent with each incremental dose of lidocaine. Clinical outcome assessment included a 10-point numeric rating, 4-point severity grading, and the pain-free time interval pre- and post-treatment.
RESULTS: Intra-arterial lidocaine was administered to three patients with trigeminal neuralgia (35-year-old woman, 57-year-old man, and 34-year-old woman). In all patients, there was a latency prolongation and amplitude reduction of R1 or R2 responses or both which was evident after 5-10 mg of lidocaine administration; a more pronounced effect was seen with increasing doses. The second and third patients reported improvement in pain severity on all scales with pain-free intervals of 5 and 3 days, respectively. There was improvement in facial hyperalgesia in all three patients in all dermatomes. All three patients' symptoms had returned to baseline severity 1 month later.
CONCLUSIONS: We found that modulation of trigeminal nerve activity via the intra-arterial route is possible based on consistent intraprocedural electrophysiologic suppression and short-term clinical improvement in patients with refractory trigeminal neuralgia.
METHODS: We administered intra-arterial lidocaine in doses up to 50 mg in the middle meningeal artery territory adjacent to the arterial branch that supplies the trigeminal nerve ganglion. We performed electrophysiologic monitoring to serially assess the latency and amplitude of R1 and R2 responses in the blink reflex before and concurrent with each incremental dose of lidocaine. Clinical outcome assessment included a 10-point numeric rating, 4-point severity grading, and the pain-free time interval pre- and post-treatment.
RESULTS: Intra-arterial lidocaine was administered to three patients with trigeminal neuralgia (35-year-old woman, 57-year-old man, and 34-year-old woman). In all patients, there was a latency prolongation and amplitude reduction of R1 or R2 responses or both which was evident after 5-10 mg of lidocaine administration; a more pronounced effect was seen with increasing doses. The second and third patients reported improvement in pain severity on all scales with pain-free intervals of 5 and 3 days, respectively. There was improvement in facial hyperalgesia in all three patients in all dermatomes. All three patients' symptoms had returned to baseline severity 1 month later.
CONCLUSIONS: We found that modulation of trigeminal nerve activity via the intra-arterial route is possible based on consistent intraprocedural electrophysiologic suppression and short-term clinical improvement in patients with refractory trigeminal neuralgia.
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