On Sun 07 Feb, Phil Gesotti wrote:
> Brian I tried attaching to the web site, but didn't have any luck.
> Could you e-mail a copy of the paper directly to a fellow engineer?
Try the attachment which is for your copy only Phil - Putting this much
data out to the list blows a lot of the older rigs right out of the water!
> Now regarding avoiding Sinemet, I guess I agree that metering the
> correct dosage is most difficult as the disease progesses. However,
> there is something that has been bothering me and that is, why should
> all the symptoms be attributed to loss of dopamine producing cells?
I usually steer away from speculation about the constituents of the
'black box': I am looking at it from the point of view of someone who
is already at the sharp end, and needs to find practical ways to live
with the situation as it is. Here are some thoughts for you to work on
while you are still an active worker- I really think that our thought
processes do slow up to some degree as PD progresses, and since the
last neuro I spoke to cheerfully told me that I must be just about
out of natural Dopamine producers, I get the feeling that I am still
driving but the petrol (Gas) tank is reading empty!!
When you read about my model of the system, you will find that I
place considerable importance to the concept of a flowing system. It
has to flow, otherwise we would be unable to introduce man-made
Sinemet into the brain. At one end of the flowing system are the
Dopamine-producing cells, and at the other are the waste products from
the natural breakdown of the dopamine. If we introduce anti-cholinergic
drugs, or MAO-B blockers, we are blocking-off some of that break -down
route, so that the surviving dopamine will last a bit longer. We then
cash that in by reducing our input of levodopa, and we MAY (I'm not
sure of this) end up with more dyskinesia margin.
Can anyone tell me about the dangers in messing with the proportions
of acetylcholine, or MAO B, or COMT ? Why were the levels of these
chemicals at their original settings anyway? Is it not possible that
by blocking this and that, we may release a more fundamental problem
in the long term?
Another point: Cabergoline's claim to fame is that it lasts so long
that it need only be taken once every 24 hours. Good news? I am not so
sure - It also means that if you get the amount wrong, you have to
suffer the consequences for 24 hours (ouch).
Now here is a real challenge for you experts: What is dyskinesia?
Yes, I know how it manifests itself, I have plenty of experience of that,
but what is actually going on inside the brain? The conventional story
is that it is some sort of a reaction to too many years of Sinemet
useage. If so, why am I still using levodopa with success after 19 years
of continuous use? How is levodopa involved? Why does it take Years to
develop?
I think Dyskinesias are another example of that endearing trick of
neurologists, where if they come across something which they don't
understand, they simply give it a latin or Greek name and pass quickly
on to the next question. So let's stand well back and look at the system
again...
I have always felt a little sensitive about the fact that my Model
defines dyskinesia as being the result of the Dopamine level exceeding
a critical value, and perhaps getting to synapses which were not the
original target, thus sending the electrical message to the wrong muscles.
My point is that I can produce plausible explanations for most of the
phenomena which we associate with dyskinesias (including the dreaded
Di-phasic Dyskinesia)
I am beginning to wonder..... You know the old saying:
If it looks like a duck, walks like a duck, quacks like as duck,
and lays eggs, then maybe, just maybe, it IS a duck.
--
Brian Collins <[log in to unmask]>
Age 59: Diag. 39: First Symptoms 33
