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A751
October 25, 2005 2:00:00 PM - 3:30:00 PM Room C301 |
| Subcutaneous Sumatriptan for Refractory Trigeminal Neuralgia: Results from a Double-Blind Placebo Controlled Crossover Trial |
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Miwako Saito, M.D., Akifumi Kanai, Ph.D., M.D., Sumio Hoka, Ph.D., M.D. Anesthesiology, Kitasato University School of Medicine, Sagamihara, kanagawa, Japan |
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Backgroung: Mechanical compression of the trigeminal root adjacent to the pons by an artery has been generally thought to cause trigeminal neuralgia. A 5-HT1B/1D receptor agonist may inhibit vasodilation and inflammation near the irritated trigeminal root. Recently, a 5-HT1A receptor agonist has been reported to attenuate mechanical allodynia in a rat model of trigeminal neuralgia. The present study was performed to examine the effectiveness of a 5-HT1A/1B/1D receptor agonist, sumatriptan, on trigrminal neuralgia. in a double-blind placebo controlled crossover study. Methods: We enrolled consecutive patients with idiopathic trigeminal neuralgia into this double-blind placebo controlled crossover study. Inclusion criteria were painful paroxysms for at least 3 months and pain intensity of more than 4 cm according to a 10-cm visual analogue scale (VAS), and the daily dose of oral drugs including carbamazepine unchanged during the 7 days prior to enrollment. Patients subcutaneously received either 3 mg in 1 ml of sumatriptan or 1 ml of saline placebo. A 7-day period was followed by a crossover treatment with sumatriptan or placebo. The order of treatments was randomized. The paroxysmal pain triggered by touching face or talking was assessed with a VAS before and 15 min after the treatment. Additionally, patients were asked to note whether the pain returned and how long after therapy it recurred. Previous conventional agents were discontinued 12 hrs before the treatment and resumed when the pain recurred or failed to relieve. Results: Twenty-two outpatients of both sexes (male; n = 3, female; n = 19), aged 34 to 89 years (mean age = 64.5 years, SD = 13.0) were enrolled. No significant differences were found between the sumatriptan and the placebo treatment regarding VAS of paroxysmal pain just before the treatment. VAS was not changed after the subcutaneous administration of saline (from 8.4±2.0 cm to 8.0±2.6 cm), but it was significantly decreased by subcutaneous sumatriptan (from 8.2±2.3 cm to 2.6±3.1 cm). The effect of the treatment was continued for 7.9±4.6 hrs. Adverse events after the subcutaneous administration of sumatriptan occurred in 5 patients: fatigue in 5 cases and nausea in 2 cases.Discussion: There is a possibility that sumatriptan provides the attenuation of the arterial compression which irritates the root entry zone of trigeminal nerve, resulting in the relief of trigeminal neuralgia. Trigeminal neuralgia presenting with severe, sustained and crescendo pain often can be difficult to treat with oral medications, because the pain can be triggered by moving mouth. In contrast, a rapid control may be achieved by the subcutaneous administration of sumatriptan without moderate or severe adverse events for patients with trigeminal neuralgia. A further study is required to assess whether the patients can attain pain relief with administration of intranasal sumatriptan using a metered-dose spray which is commonly used in migraine patients at home rather than a clinical enviroment. Anesthesiology 2005; 103: A751 |