Posted by Miguel (18.104.22.168) on September 25, 2000 at 20:21:13:
In Reply to: Nerves posted by Bennie Sue on September 25, 2000 at 18:00:52:
My understanding of the pain mechanism is somewhat
limited. Vasodilation and vasoconstriction do not
Here is where it becomes shaky...Nerves usually run
parallel to blood vessels. Pain comes from transmission
of sensation via nerves. I imagine that the
vascular response elicited during an attack is
being interpreted by the body as a negative incidence
since it is happening due to an imbalance, i.e.:
serotonin levels, etc. The body then responds by
platelet aggregation at the site of the injury.
Platelets release several things, PGI among them.
PGI is prostaglandin, and it causes the pain.
The interesting aspects of this problems are:
Why does the body feel that the vasodilatory response
is one that merits platelet aggregation? Vasodilation
and vasocontriction are normal events. Consider that if
vasodilation was an anormality, when we went for a
jog, or had a couple of drinks our whole body would
respond in the tremendous pain experienced during CH
because of the vasodilatory response.
This type of response may point then at the possiblity
of tisse damage, hence the response we get. Not long
ago someone posted here that they had read somewhere
something about myelin sheet damage associated with
CH. I could understand that as possibly the cause
for the platelet aggregation and PGI release. The
vasodilatory response is so exagerated that it affects
the myelin sheet covering the nerve running parallel to
the blood vessel that is dilating.
Another aspect of if might be directly related to
serotonin. As large amounts of serotonin are secreted
during an attack, they permeate from the nerve to the
vascularture in the cortex. Platelets are apparently the
carriers for serotonin. Platelets come to the site
where the serotnin "leak" is taking place to pick it up
and dispose of it, or carry it elsewhere in the body.
Platelets then release PGI during the "pick up", hance the localized
A thrid option - IL2 secretion by macrophages.
Macrphages are called upon the affected area to
repair the blood vessel stretching beyond normal
levels. Macrophages "gobble up" dead cells in the
area while secreting IL2 in very large amounts to repair
the damage. Damaged cells may likley be endothelial
cells that become damaged due to excessive dilation
of the vessel. This may also contribute to increased
leakage of serotonin and other agents accros the
blood vessel wall since the protective linning of
the blood vessel might be damaged.
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