Acute migraine headache: possible sensitization of neurons in the spinal trigeminal nucleus?

Abstract

Neurology. 2002;58:1234‐1238.OBJECTIVE: To investigate trigeminal sensory processing in patients with migraine using a novel “nociception‐specific” blink reflex. METHODS: Seventeen patients with unilateral migraine headache were studied within 6 hours of onset. Blink reflexes were elicited with a standard stimulating electrode (standard blink reflex) and concentric stimulating electrode (nociception‐specific blink reflex) during the acute migraine attack, after treatment with IV lysine acetylsalicylate (1,000 mg) or oral zolmitriptan (5 mg) and interictally. RESULTS: After standard stimulation, no differences were detected for the R1 and R2 onset latencies and areas under the curve (AUC) between the different time points and the headache and nonheadache side. Nociception‐specific stimulation revealed a shortening of R2 onset latencies (44.3 ± 5.4 ms for headache side vs 48.9 ± 5.8 ms for nonheadache side) during the acute migraine attack compared with the headache‐free interval (49.8 ± 5.3 vs 49.8 ± 4.5 ms). The AUC of the R2 increased on the headache side by 680% and on the nonheadache side by 230% compared with the headache‐free interval. Drug treatment parallel to pain relief increased the onset latencies (zolmitriptan: 48.0 ± 8.2 ms for headache side vs 52.3 ± 7.6 ms for nonheadache side; lysine acetylsalicylate: 48.0 ± 5.0 ms for headache side vs 51.2 ± 5.6 ms for nonheadache side) and reduced the AUC of R2 (zolmitriptan by 45% and lysine acetylsalicylate by 48%). CONCLUSION: The data suggest temporary sensitization of central trigeminal neurons during acute migraine attacks. Comment: This abstract from Dr. Chris Diener's group reports large changes in the AUC for onset latencies between headache affected and nonaffected sides. Drug treatment effects were small. No statistical comparisons were reported. This noninvasive technique may be useful in further exploring the mechanisms which underlie the temporary sensitization of central trigeminal neurons during acute migraine attacks. DSM