theophilus.samuels at btinternet.com
Fri Feb 9 19:28:03 EST 2001
The underlying pathophysiology is still only partly understood. In
classical migraine, the aura is traditionally believed to be due to
intracerebral vasoconstriction. However, it is more likely to be caused by
waves of depolarisation spreading across the cerebral cortex because of the
vascoconstriction. Following this, vasodilation occurs, particularly of
extracerebral vessels in the scalp and dura and is thought to produce the
headache. At the moment, there exists some evidence for the involvement of
serotoninergic pathways along with vasoactive neuropeptides. Remember, there
are no pain nerve endings (nociceptors) within the brain parenchyma, they
are only found in the covering dura (the main reason why neurosurgeons can
operate on the brain of a conscious subject, i.e. during a bilateral
pallidotomy in PD).
The management of migraine involves simple environmental changes to using
novel selective serotonin (5-HT1) receptor agonists such as sumatriptan. A
potent vasoconstrictor called ergotomine may be used, however, it has some
serious side-effects (as does sumatriptan, indeed combined use of these
drugs is contraindicated). So basically, treatment is aimed at altering
serotonin levels or causing vasoconstriction. Note, that simple analgesics
such as paracetamol or aspirin can be given initially (as soluble
preparations) and should really be taken with an antiemetic such as
'Who's that guy standing behind you?'
MS <marshmallow5 at yahoo.com> wrote in message
news:6m4g6.452$WV5.59220 at news1.news.adelphia.net...
> Can anyone explain whether migraine involves vasoconstriction and/or
> vasodilation? Also, what is the mechanism of anti-migraine medication?
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