Brain, Vol 121, Issue 7 1231-1237, Copyright © 1998 by Oxford University Press
A May, SL Shepheard, M Knorr, R Effert, A Wessing, RJ Hargreaves, PJ Goadsby and HC Diener
High-intensity electrical stimulation of the trigeminal ganglion is
accompanied by mast cell degranulation, vasodilatation, increased
endothelial permeability and leakage of albumin from postcapillary venules
within the dura mater. Overall, the histological appearance suggests an
evolving sterile inflammatory response. This neurogenic inflammation within
the meninges has been suggested as a model to explain the pain in migraine
and cluster headache, and has been used to characterize the pharmacology of
anti-migraine compounds. Using the rat model of neurogenic inflammation,
the albumin extravasation ratio (stimulated : unstimulated side) in
vehicle-treated animals in the dura and retina was 1.60 +/- 0.11 and 1.76
+/- 0.18, respectively (n = 10; values are mean +/- SEM). Pretreatment with
sumatriptan (n = 9) produced a highly significant reduction in the ratio of
extravasation within the dura to 1.10 +/- 0.06 (P = 0.002) and in the
retina to 0.96 +/- 0.06 (P = 0.001), as did the neurokinin-1 receptor
antagonist RP 67580 (n = 12) in the dura (1.04 +/- 0.11, P = 0.002) and
retina (1.08 +/- 0.06, P = 0.001). These data demonstrate increased
endothelial permeability and leakage of albumin not only in the dura but
also in the retina. In a second stage we investigated possible
extravasation in the human retina in acute migraine (n = 8) and cluster
headache (n = 5) using fluorescein or indocyanine angiography. No increased
endothelial permeability or leakage of dye could be found in the human
retinal or choroidal vessels during headache attacks or in the
headache-free interval in persons suffering from both migraine and cluster
headache. These data raise the possibility that neurogenic inflammation is
not a major factor in headache attacks in migraine or cluster headache.
ARTICLES
Retinal plasma extravasation in animals but not in humans: implications for the pathophysiology of migraine
Institute of Neurology, London, UK. amay@ion.ucl.ac.uk
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