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3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache

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

European Journal of Neurology

|July 21, 2009

Summary

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.

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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.