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Steve

I have  long failed to understand the role of dopamine in PD but then my
education has been in the social, not biological, sciences.

I ask:

How do they know I'm lacking dopamine when there is no blood test to measure
how much I have? (and  I don't want to wait til I die to find out)

Why if lack of dopamine caused my tremors do leads in my brain that
constantly transmit electric impulses from neurotransmittters in my chest
stop them?  And how was  DBS able to immediately straighten out my dystonic
foot?  Since DBS 4 ago years I've kind of plateaued except for my voice.

I don't think the disease process is understood at all, even  though they
say it is, but then what do I know?

And I don't buy that  you've lost 80%  of your dopamine before you become
symptomatic.  If lack of  it is the cause, how do you function so long
without the right  amount whatever that might be?

Why do PD meds affect people so differently?  A few years ago Edith Love and
Mario attempted to develop a  data base to share info.  We need something at
least nationally.

Ray

Rayilyn Brown
Board Member AZNPF
Arizona Chapter National Parkinson's Foundation
[log in to unmask]
----- Original Message -----
From: "Steve Rack" <[log in to unmask]>
To: <[log in to unmask]>
Sent: Monday, June 18, 2007 8:31 PM
Subject: barking up the wrong tree


> Ray I'm going to go out on a scary limb here. Dopamine is a
> neuro-transmitter, one of many identified in our brain. Highly
> specialized chemicals these - each with a specific task - except (it
> seems) dopamine. Dopamine is the transmitter of mood and movement. Or
> is it? I don't know of another dual purpose neuro-transmitter. Do
> you? Perhaps there's a fundamental reason that sinemet and the
> agonist drugs give us strange side effects before losing what
> effectiveness they had and failing entirely. Have our researchers
> been barking up the wrong tree?
> --
> Steve Rack
>
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