Paula,

From all I've read, a cholinisterase inhibitor is an enzyme which inhibits the breakdown of acetylcholine. In other words, our bodies naturally produce this enzyme and drugs like Aricept interfere with the enzyme either blocking it or dampening it, so acetylcholine does not break down. In PD, we already have too much of it, so in essence using something like Aricept leave us with even more which could result in more dystonia! Is this what you are wondering?

To your question...

we know that acetylcholine is used in chemical warfare, so would the enzyme prevent the acetylcholine from a chemical attack from getting processed? it is offering some kind of protection that we haven't learned about yet, it seems. This is a contradiction to me so I need help with it.

The drug or chemical warfare blocks the enzyme from breaking down acetylcholine; it does the opposite, it allows the acetyl-ch to proliferate unchecked. The enzyme is like a bouncer at a bar keeping things in check, by giving the bouncer the night off (the cholinesterase inhibitor), the bar is over run with too much drunken acetyl choline- I'm bad with analogies, but you get it. In war we end up with cholinergic toxidrome or toxicity (too much acetyl choline) which can result in death.

This info and research I put together is buried in another post; I am going to copy/paste it here. Also, the common sense idea about this aggravating our symptoms has been corraborated by a pharmacist and by research. Next, I ask, do our doctors have any common sense?

From my other post:

Fairly recently, it has become in vogue for neuros to prescribe cholinesterase inhibitors used routinely for Alzheimer's to treat cognitive impairment for PD. However, you should ask your neuro many questions before doing so because they directly counteract the effect of any other PD drugs we may take and further screw with what little neurotransmitters we have left. We have dissected this in another recent long thread, but this is the gist of it all:

-PD results in loss of dopamine and a subsequent increase in acetylcholine; the latter is what causes our motor symptoms: bradykinesia, tremor, and rigidity.

-Taking a cholinesterase inhibitor actually raises our levels of acetylcholine when we already have too much. Common sense would tell us that this will exacerbate our Parkinson's symptoms. Sure enough, there are studies to substantiate this:

From PubMed:

Cholinesterase inhibitors: tremor and exacerbation of Parkinson's disease.

[No authors listed] Prescrire Intl

(1) Three cholinesterase inhibitors are marketed in France for the treatment of Alzheimer's disease: donepezil, galantamine and rivastigmine. Tremor and dystonia are known adverse effects of cholinesterase inhibitors. (2) In patients with Parkinson's disease who have cognitive disorders, or in patients with Lewy body dementia, exacerbations of parkinsonism and tremor have been observed during treatment with cholinesterase inhibitors at normal doses. The disorders were reversible on withdrawal of the cholinesterase inhibitor. (3) Withdrawal of cholinesterase inhibitors should be considered if gait disorders, falls or parkinsonism occur or worsen during treatment.


-To further confound our treatment, neuros do this when we are already taking anticholinergics like Amantadine to lower the acetylcholine levels. Why would they give us another drug that then increases it? Doesn't this seem counterintuitive?

-Finally, from the DSM IV:

e. Mild cognitive impairment

The term "mild cognitive impairment" describes a heterogeneous group of individuals, with some patients in the earliest stages of Alzheimer's disease and others suffering from other conditions. There are no FDA-approved medications for the treatment of mild cognitive impairment at this time. Clinical trials of cholinesterase inhibitors for mild cognitive impairment have enrolled a narrower and better defined population of patients with mild cognitive impairment than most clinicians actually treat in practice, but even with these well-defined patients the evidence from clinical trials supporting use of cholinesterase inhibitors is weak (172, 173). Given the inconclusive data, the potential safety concerns that exist with this class of medications in this patient population, and the lack of FDA approval for this indication (reviewed in Sections V.B.1.a.4 and II.C.5.a.1.a), no specific recommendation can be made in favor of routine use of cholinesterase inhibitors in patients with mild cognitive impairment at this time. Nonetheless, individual patients may benefit from their use.

Not sure about Lindy' s patch; I'd like to know too. Hope I'm not thread-jacking...trying to help

Laura