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| 50th Annual Meeting of the American Headache Society |
Boston, Massachusetts June 26-29, 2008 |
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Role of Vascular Endothelium in Migraine |
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BY MAURY M. BREECHER
Contributing Writer |
BOSTON — After accepting this year’s Seymour
Solomon Award, Dr. Gretchen Tietjen presented the
Seymour Solomon Presidential Lecture, “The Role of the
Vascular Endothelium in Migraine” on June 26 during the
50th Annual Scientific Meeting of the American Headache
Society.
Dr. Tietjen of the University of Toledo Medical Center
pointed out that the vascular endothelium is an
important organ involved in many dysfunctions including
migraine. Other associated conditions include Reynaud’s
disease, pre-eclampsia, sleep disorders, hypertension,
retinopathy, angina, and stroke.
The endothelium has regulatory functions such as
vasodilatation, thrombolysis, platelet disaggregation,
anti-proliferation, and anti-inflammation. However,
there is also a balance between the endothelium and
factors associated with diseased endothelium. It also
moderates vasoconstriction, thrombosis, adhesion
molecules, growth factors, inflammation, and oxidant
activity. In other words, the endothelium responds to
its environment.
According to Dr. Tietjen, studies in Turkey show that
migraineurs can have impaired endothelial dilation with
migraine. Oxidative stress impacts endothelial
dysfunction causing activation of inflammation,
thrombosis, proliferation, and impaired vaso-reactivity.
Many substances have dual roles on the endothelium, Dr.
Tietjen pointed out. For instance, if given to a healthy
endothelium, serotonin and acetylcholine cause dilation.
However, if they are given to a diseased endothelium,
they will cause vasoconstriction.
“You can get endothelial activation with inflammation,
thrombosis, and muscle proliferation, and you can get
impaired vascular activity,” said Dr. Tietjen. “It’s all
mediated through oxidative stress. Many of the
inflammatory components, such as those that cause
thrombosis, can also then lead back to oxidative stress.
It’s sort of a positive feedback loop.”
Dr. Tietjen reported that Vanmolkot and his colleagues
did a comparison of arterial diameter in migraineurs
versus controls and found arterial diameter was more
impaired in the migraine population (Neurology.
2007;68:1563–1570).
“What this suggested is that within the group of
migraineurs they examined, compared to a control group
of healthy people without migraine, was they had
systematic endothelial dysfunction,” explained Dr.
Tietjen. “These were not people who had migraines for a
long time, yet they still showed endothelial
dysfunction.”
She noted that markers of endothelial dysfunction (ED)
include altered vascular reactivity and assorted
clinical (Livedo Reticularis or LR), genetic, and
radiological markers. LR is associated with migraine in
women and may be a clinical marker for increased stroke
risk in migraineurs (Headache. 2002;42:263-267).
Another marker of ED is Von Willebrand Factor (vWF). vWF
is higher in migraineurs than in the non-migraine
controls, according to Dr. Tietjen’s studies (Neurology.
2001;57:334-336).
Dr. Tietjen and colleagues looked at vWF in comparison
to upstream and downstream ED markers and found vWF
activity levels predicted markers for
oxidative stress, platelet aggregation, decreased
fibrinolysis, increased inflammation, and vascular
reactivity (using transcranial Doppler).
So the question is does ED cause migraine? Or does
migraine cause ED?
There is evidence on both sides, according to Dr.
Tietjen. For instance, evidence that ED causes migraine
includes the fact that ED presents early in the course
of migraine (Neurology.2007;68:1563-1570). Dr. Tietjen
summarized that migraine is associated with endothelial
dysfunction and many treatments for ED lessen the
headache disorder. |
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