no rush....thanks!
p

Paula,

I'm trying to come to terms with all these terms too

I understand in a general way how neurotransmission works but needed a visual to fine tune it for me.

I found a really good, clear explanation here with images. http://www.holisticonline.com/Remedi...n/pd_brain.htm

From their site:

In a healthy brain,

During movement, signals pass from the brain's cortex, via reticular formation and spinal cord (pathway A), to muscles, which contract. Other signals pass, by pathway B, to the basal ganglia; these damp the signals in pathway A, reducing muscle tone so that movement is not jerky. Dopamine, a nerve transmitter made in the basal ganglia, is needed for this damping effect. Another transmitter, acetylcholine, inhibits the damping effect.

In Parkinson's disease, degeneration of parts of the basal ganglia causes a lack of dopamine within this part of the brain. The basal ganglia are thus prevented from modifying the nerve pathways that control muscle contraction. As a result, the muscles are overly tense, causing tremor, joint rigidity, and slow movement. Most drug treatments increase the level of dopamine in the brain or oppose the action of acetylcholine.

Paula, I've looked at a few sites, and if I understand this correctly. Due to loss of dopamine we end up with too much acetylcholine and this imbalance leads to the primary symptoms of tremor, rigidity, and bradykinesia. This is why we are prescribed things like Amantadine (anticholigernic) to help modulate this imbalance. See Parkinson's Hope Digest for more info.

An acetylcholinesterase inhibitor like Aricept works to stop an enzyme from breaking down acetylcholine and thus increases their level and function in our brain chemistry. In other words, we already have too much of it to begin with, so our neuros might prescribe Artane or Amantadine, then we are given Aricept which undoes the other two. I just think that given the chaos that ensues when we lose so much dopamine, neuros should be extra careful about messing with the interplay of our remaining neurotransmitters. Especially when it seems like for any given movement we may need more of one neurotransmitter over the other - these drugs are not given sustainably and can't be applied evenly or adjust to what levels are needed from hour to hour. It seems like this could cause even more problems for us, especially given Zucchini Flowers observation with taking Artane.

Not quite sure yet what all this means for dementia. Other than AD = too little acetyl and PD = too much

Hope this helps a little.

Laura

Thanks Laura,

We agree in our interpretations and thanks for the resources you are providing. I didn't realize Amantadine was such a major player. I'm going to research it next. I've been trying to wean off Amantadine since the addition of nortriptyline but it's a no go......instant dyskinesia...another myth [it only works for 6 mos.]......Amantadine works for years, not six months. Rigidity also increases without it for my type of PD, whatever it may be.

It appears that symptoms of pd result from too much acetylcholine as much as lack of dopamine.

Tossing genetics in for the heck of it. I wonder what genes are at work here?

oh i wanted to mention that the article you cited at
http://parkinsons.hopedigest.com/art...mical_ensemble

was written by a patient....Matt Nilsen, which likely is the reason we can understand it.

paula

The wikis for 'anticholinergic' and 'acetylcholine' are easy to understand, but perhaps they have already been a first port of call.....

http://en.wikipedia.org/wiki/Anticholinergic

http://en.wikipedia.org/wiki/Acetylcholine

A neuropsychiatrist I used to see seldom missed an opportunity to challenge my taking 4 mg Detrol daily for incontinence. To me this little pill makes the difference between leaving the house occasionally and living in the bathroom.
The reason the neuropsychiatrist objected was that Detrol is an anticholinergic, and anticholinergics contribute to dementia.

At the same time, a neurologist I used to see prescribed Amantadine for dyskinesia, and even boosted the dose from 100 to 300 mg ovenight. I can't get off of it, either, even though I hate it--fogbrain and black visual patterns go with it. I was afraid to ask about the dementia angle, because otherwise the neurologist was pushing me to get a DBS with only minor dyskinesias.

I'm even more afraid of neurologists in general now, but that would make it a long story.

Jaye

Jaye,
I was on oral anticholinergic for incontinence, for several years, it stopped working and so I stopped taking it, and of course symptoms re-emerged, awful. Am now using Kentera patches (oxybutynin) which have got me back to where I was, with fewer unwelcome effects.

Lindy

Well, break it to your doctors gently but the mechanism of Amantadine on pd remains unknown and it is listed separately from anticholinergic drugs.

http://www.scribd.com/doc/24033066/A...ticholinergics

http://www.ncbi.nlm.nih.gov/bookshel...ons&part=A3600

not much has changed in the time span between these two publications.

paula

Paula,

Thank you for clarifying the drug class of Amantadine; I forget that it is not truly an anticholinergic. Also, the book you link to is a good resource for reviewing drugs in great detail and from a historical perspective. I am beginning to note that many times I read what amounts to myth on drugs that have been around for some time, like Levodopa efficacy over the long term, disease progression and drugs, etc. This has given me some peace of mind.

So, with Amantadine acting as an anticholinergic...I wonder if it can really then be lumped with other drugs firmly in that class as showing a more rapid decline in mental function?

I also wonder if many of us need a combo of Amantadine or anticholinergic and dopa stimulation (agonists or levodopa) based on subtypes? In other words, if you are more rigid should you have more of an anticholinergic and less levodopa? I wonder if playing around with these drugs to restore more of a natural balance is more beneficial to us in both symptom control and longer term efficacy of drug treatment?

Laura

Great site! It's worth the short registration.
you can comment and participate.

http://www.thedoctorschannel.com/

http://www.thedoctorschannel.com/vid...html?specialty=

http://www.thedoctorschannel.com/vid...html?specialty=

http://www.thedoctorschannel.com/dueling_doctors/

much more


Here's where i found the link. This is the journal for Particpatory Medicine for which we are submitting an article. See video...and then go to doctors internet tv channel...both sites are fabulous. Can we find some medical allies here? videos above are about nortriptyline and cholinesterase inhibitors

http://participatorymedicine.org/

whos involved:
The Society’s Board of Directors

Alan Greene, MD, President
Cheryl Greene
Dan Hoch, MD
Danny Z. Sands, MD, Co-Chair
Dave deBronkart (e-Patient Dave), Co-Chair
Gilles Frydman, Vice President
Joe Graedon
John Grohol, PsyD, Treasurer
John Lester
Jon Lebkowsky
Sarah Greene
Teresa Graedon, Secretary

paula

Paula,

You may not want to see any more sites on dementia but wanted to quickly add this one, just in case...particularly there are 3 types for PD and there is no set criteria for defining PD dementia- big surprise, in as much as everything else for us seems to be clear as mud.

eMedicine : PD Dementia

Laura