james at teoth.fsnet.co.uk
Thu Feb 8 18:49:11 EST 2001
On Wed, 07 Feb 2001 04:41:38 GMT, "MS" <marshmallow5 at yahoo.com> wrote:
>Can anyone explain whether migraine involves vasoconstriction and/or
>vasodilation? Also, what is the mechanism of anti-migraine medication?
Let me first state that the following is only the prevailing theory of
migraine and in no way represents fact since most migraine researchers
acknowledge that there is alot we don't know about migraine.
The visual auras and disturbances of conscioussness of the various
migraine subtypes is believed to be a result of intracerebral
vasoconstriction causing areas of the brain to become momentarily
depolarised, creating the symptoms of the first phase. There is no
pain in the first phase.
The second phase results from reflex vasodilation of all cranial
vessels including the extracranial ones. This extracranial
vasodilation is the cause of the pain, and the symptom that migraine
sufferers complain of. Again, I must stress that the above is all
speculation as there is no real evidence for any of the above.
Migraine drugs fall into two groups: treatment drugs and prophlaxis
drugs. Treatment drugs are used in the acute phase and consist mainly
of 5HT agonists which promote vasoconstriction in the second phase.
Prophlaxis drugs act to reduce the incidence of any attacks and there
are many classes: fancy 5HT antagonists, antidepressants,
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