TY - JOUR

T1 - Prednisolone reduces nitric oxide-induced migraine

AU - Tfelt-Hansen, P

AU - Daugaard, D

AU - Lassen, L H

AU - Iversen, H K

AU - Olesen, J

AU - Tfelt-Hansen, P

AU - Daugaard, D

AU - Lassen, L H

AU - Iversen, H K

AU - Olesen, J

N1 - Keywords: Adult; Analysis of Variance; Blood Flow Velocity; Cerebrovascular Circulation; Cross-Over Studies; Double-Blind Method; Female; Humans; Male; Middle Aged; Migraine without Aura; Nitroglycerin; Pain Measurement; Prednisolone; Severity of Illness Index

PY - 2009

Y1 - 2009

N2 - BACKGROUND AND PURPOSE: Glyceryl trinitrate (GTN) induces delayed migraine attacks in migraine patients. The purpose of this study was to investigate whether pre-treatment with prednisolon could decrease this effect of GTN. METHODS: In this double-blind, randomized and placebo-controlled, crossover study 15 migraineurs with migraine without aura were pre-treated with 150 mg of prednisolone or placebo followed by a 20-min infusion of GTN (0.5 ug/kg/min). One hour after the GTN-infusion, the participants were sent home, but continued to rate headache and possible associated symptoms by filling out a headache diary every hour for 12 h. There were two equal primary efficacy end-points: frequency of delayed migraine and intensity of delayed headache. RESULTS: Nine patients experienced a GTN headache fulfilling the diagnostic criteria for migraine without aura on the placebo day compared with four patients on the prednisolone day (P = 0.14). Prednisolone pre-treatment did not alter the summed or peak immediate headache responses to GTN significantly (P = 0.08, P = 0.07), whereas the peak headache scores during the following 12 h were significantly lower after prednisolone pre-treatment (median peak score = 1, range 0-8) compared with placebo (median = 4, range 0-8) (P < 0.01). There was no difference between the two treatment days in the effect of GTN on blood flow velocity of the middle cerebral artery (a decrease) or on the dilation of the superficial temporal artery or the radial artery. CONCLUSION: Pre-treatment with prednisolone did not reduce the immediate GTN-induced headache, did not inhibit the frequency of delayed headache but significantly decreased the intensity of delayed GTN-induced headache. These findings suggest that GTN causes induction of inflammatory mediators, and that this is the mechanism of delayed GTN-induced migraine. They also support a role of inflammatory mediators in spontaneous migraine attacks.

AB - BACKGROUND AND PURPOSE: Glyceryl trinitrate (GTN) induces delayed migraine attacks in migraine patients. The purpose of this study was to investigate whether pre-treatment with prednisolon could decrease this effect of GTN. METHODS: In this double-blind, randomized and placebo-controlled, crossover study 15 migraineurs with migraine without aura were pre-treated with 150 mg of prednisolone or placebo followed by a 20-min infusion of GTN (0.5 ug/kg/min). One hour after the GTN-infusion, the participants were sent home, but continued to rate headache and possible associated symptoms by filling out a headache diary every hour for 12 h. There were two equal primary efficacy end-points: frequency of delayed migraine and intensity of delayed headache. RESULTS: Nine patients experienced a GTN headache fulfilling the diagnostic criteria for migraine without aura on the placebo day compared with four patients on the prednisolone day (P = 0.14). Prednisolone pre-treatment did not alter the summed or peak immediate headache responses to GTN significantly (P = 0.08, P = 0.07), whereas the peak headache scores during the following 12 h were significantly lower after prednisolone pre-treatment (median peak score = 1, range 0-8) compared with placebo (median = 4, range 0-8) (P < 0.01). There was no difference between the two treatment days in the effect of GTN on blood flow velocity of the middle cerebral artery (a decrease) or on the dilation of the superficial temporal artery or the radial artery. CONCLUSION: Pre-treatment with prednisolone did not reduce the immediate GTN-induced headache, did not inhibit the frequency of delayed headache but significantly decreased the intensity of delayed GTN-induced headache. These findings suggest that GTN causes induction of inflammatory mediators, and that this is the mechanism of delayed GTN-induced migraine. They also support a role of inflammatory mediators in spontaneous migraine attacks.

U2 - 10.1111/j.1468-1331.2009.02654.x

DO - 10.1111/j.1468-1331.2009.02654.x

M3 - Journal article

VL - 16

SP - 1106

EP - 1111

JO - European Journal of Neurology

JF - European Journal of Neurology

SN - 1351-5101

IS - 10

ER -