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Updated: Jun 21, 2026

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache
Published on: June 2, 2014
Prednisolone reduces nitric oxide-induced migraine
P Tfelt-Hansen1, D Daugaard, L H Lassen
1Department of Neurology, Danish Headache Centre, University of Copenhagen, Glostrup Hospital, Glostrup, Denmark. ptha@glo.regionh.dk
Prednisolone pre-treatment did not prevent delayed headaches from glyceryl trinitrate (GTN) but significantly reduced their intensity. This suggests inflammatory mediators play a role in GTN-induced migraine.
Area of Science:
- Neurology
- Pharmacology
Background:
- Glyceryl trinitrate (GTN) is known to trigger delayed migraine attacks in susceptible individuals.
- The potential of pre-treatment with corticosteroids to mitigate GTN-induced migraines requires investigation.
Purpose of the Study:
- To evaluate the efficacy of prednisolone pre-treatment in reducing GTN-induced delayed migraine attacks.
- To explore the underlying mechanisms of GTN-induced headaches.
Main Methods:
- A double-blind, randomized, placebo-controlled, crossover study involving 15 migraineurs without aura.
- Participants received either prednisolone or placebo, followed by a GTN infusion.
- Headache intensity and frequency were monitored hourly for 12 hours using headache diaries.
Main Results:
- Prednisolone did not significantly alter the frequency of immediate or delayed GTN-induced headaches.
- A significant reduction in the peak intensity of delayed headache was observed following prednisolone pre-treatment (P < 0.01).
- GTN's effects on cerebral blood flow velocity and arterial dilation were not significantly altered by prednisolone.
Conclusions:
- Prednisolone pre-treatment significantly decreases the intensity of delayed GTN-induced headache, suggesting a role for inflammatory mediators.
- The findings support the hypothesis that inflammatory mediators are involved in the mechanism of delayed GTN-induced migraine.
- These results may also imply a role for inflammatory mediators in spontaneous migraine pathogenesis.
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