Posted by Miguel (22.214.171.124) on September 18, 2000 at 10:09:26:
The following are the results from two posts below. Differences
fromt he analyzed (in-part) data with your condition
do not in any way imply that you suffer or do not suffer
from the CH syndrome. Such determinations must be
made by a board approved physician. Additionally,
the expression of conditions surveyed among sufferers
do not explicitly mean that a person may suffer one type
of CH over another, nor that there is a norm of conditions
currently exisiting and historical, which may predispose
a person to suffer CH. CH is a complex syndrome. The
variability in this data expresses exactly that. At this point
conclusions based on the small population examined
are not, and can not should be drawn.
There are still 10% of the respondents to complete the
survey with the episodic/chronic part of the response.
This is within physiological error, thus the data can be
studied and compared to standards for these conditions.
Those respondents are included in the overall data.
However, they can not be included at this point in the
"CH Type" data.
Total Responders: 29
Currently Episodic: 15 (52%)
Currently Chronic: 11 (38%)
Unassigned Episodic/Chronic: 3 (10%)
Episodic Turning Chronic (included as currently chronic above): 3 (10%)
34% Have Low, or lower than normal resting Blood Pressure.
45% Have familial history of depresion/epilepsy/psychosis.
Interestingly enough, most respondents indicating
a specific response to question #2 (depression, epilepsy,
psycosis) indicate a history of depression in their family,
and a few epilepsy. No respondents noted psychosis in their
34% Have familial history of CHF.
DATA BY CH TYPE
40% Have low, or lower than normal resting Blood Pressure
53% Have familial history of depresion/epilepsy.
47% Have familial history of CHF.
27% Have low, or lower than normal resting Blood Pressure
45% Have familial history of depresion/epilepsy.
27% Have familial history of CHF.
Overall, it seems that familial history of mental disease, as
associated with 5-HT and 5-HT receptors, is one common
trend among episodics and chronics, with very similar
number of respondents expressing largely a familial
history depression, followed in number by a history
of epilepsy in the family.
Perhaps the most striking differences become evident
once the population surveyed is divided by its type
of CH, chronic v. episodic. Would a history of familial
CHF, or low resting blood pressure be a determinant, or
at least a contributing factor to determine if a person
becomes or is chronic from the onset of the syndrome?
May be, perhaps not. However, episodic's data show that
40% of the respondents have resting blood pressure lower
than the standard. Of course, standards are made of
above the average, average and below the average numbers.
Never the less, episodics note by almost twice the number of
chronics that their resting blood pressure is considered
below normal. Also, one episodic turned chronic (3.3% of the chornics)
notes that low resting blood pressure is part of the
picture in the individual's life.
The responses to a familial history of CHF offer
another striking difference between episodics and
chronics. Once more, episodics offer data indicating
that they have almost twice the incidence of CHF in their
families, as compared to chronics.
Blood pressure, simplistically noted, is the result of
resistence to blood flow from micro-vessels/capillaries.
Sometimes, TPR (Total Peripheral Resistence) is utilized
to note the condition of a cardiovascular system in a
systemic approach. 5-HT appears to exert its effects
on the vasulcature through G-protein mediation. Most
vasodilators do as well. Would this mean that G-protein
regulation could be a target for CH? Perhaps, as another
interim patch to improve the quality of life of those
affected by CH.
Many sufferes noted that while their resting blood pressure
was normally "low", it seemed to increase during an attack.
Many physiological pathways can contribute to that. The
"spike" in resting blood pressure may be directly related
to CH, or it might not. Considering the amount of
emotional and physical stress that an attack brings to
the sufferer, it could be very well that the change in resting
BP is the result of the stress involved in the attack,
either mediated via catecholamines, or some other of
norepinephrine-dependent response related to the disconfort
and duration of the attack. Also, it could be that our levels
of 5-HT are normally high (for episodics), maintaining
systemic vasodilation, hemostasis, and lower TPR levels.
Concomitantly, these levels maintain the brain's
cortical blood vessels constricted. G-protein-mediated
vascular responses appear to be exactly the oposite
in brain vasculature as they are for the rest of the body.
As the brain's cortical blood vessels dilate due to
a decrease in 5-HT, or an increase in MAO, or some
other 5-HT metabolizing agent, the rest of the vascualture
undergoes constriction, thus an increase in TPR.
With that said, the one can speculate even further by
noting that it is ossible that agents such as LSD and
psilocin act on the MAO, or other 5-HT-metabolizing enzyme
rather than on the 5-HT receptor itself. This would
result in increased 5-HT plasma levels as well, dilation
of the periphery and constriction of the brain's cortical
blood vessels. Just speculations and thoughts, but something to chew
5-HT is an extremely important molecule, which plays many
roles in human physiology. The article that BobP (an
excellent one, I must add) referred to in his post
explains many of the roles of 5-HT and the 5-HT receptor
in human physiological function autoregulation. Some
may now understand why I ask many of the things that at
times may seem unrelated, or perhaps too abstract (even
absurd). They relate to the 5-HT receptor and 5-HT
itself, as it affects our physiology.
There appears to be a connection between 5-HT, brain function
(depression, epilepsy, psycosys, compulsory behavior, suicide,
etc), and vasculature. Our knowledge of these phenomena is
extremely basic at this point, even from the professional
point of view. It is not only limited to a freak/extreme
vasodilation of an isolated blood vessel in the brain, or
a malformed/unusual hypothatlamus, but mostly related to
why does it happen.
Hypothalmic surgery is not feasible at this point. Even if
it was, the question would be; what do we do, and how
much of it should be done? So, what can be done at this point?
It is obvious that cardiovascular well being is paramount.
Also, that mental health is another very important factor
in CH. Because of the data, and the risks associated with
the diseases and conditions surveyed for, considering
living the healthiest life possible, mentally and physically
is obviously the best we can do right now, beside pharmacological
approaches. Yes, the pain will still come. However,
would we fight it better under sound mind, sound
vasculature conditions? I bet we would. There is no
"magic bullet" to treat CH yet. There will not be one
for many years to come, perhaps there will never be one.
This means that in most cases it is up to us and us alone to
find ways, even through home remdies, that will help us
deal with this syndrome. It is up to us alone to share
the information we have to contribute to the well being of
the affected. It is up to us alone to do away with denial,
stigma and the focus on the aberrant inefective treatments
as the norm for that treatment, as well as specific
symptoms and their exceptions to collaborate toward
a better quality of life. The quality that we are due
because of our efforts to make it so.
Once More: These numbers, although based on a small population, need
to be compared against national and world statistics regarding
what the averages or percentages of the population suffer
from the above noted aflictions in order to have statistical
validity as aberrant condtions unique, or associated with CH.
Any suggestions or help in finding sources for such data is greatly
appreciated. May post links, or e-mail me recommendations
(Likely drawing too many conclusions from too little data)
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