[QUOTE=johnt;868199]Coincidently I've been on antibiotics for the past week:
1x500mg, Flucloxacillin four times a day;
2x250mg, Penicillin V, four times a day.
(I'm taking them to help fight a foot infection.) The last week has been one of my best PD-wise for months: looser, more lively, better balance (but, still bad tremor).

My side-to-side tap test scores, at least 12 hours after my last dose of levodopa (but still benefitting from the controlled release agonist) have averaged about 36, as opposed to my normal 30.
( The results come from:
http://www.parkinsonsmeasurement.org...eToSideTap.htm
The figures given are the sum of left hand and right hand movements, with each measured over 30 sec.)


Thanks for adding to the data and its interpretation. First, the dead neurons view is, as I understand it, by no means the slam dunk that we are told it is.
Second, the bacterial theory requires the presumptions of an unidentified bacterium in the gut producing an undetected toxin capable of penetrating the BBB and interferring with dopamine for an indefinite time before being either neutralized or killing only neurons in the SN etc. Too messy. Contrast it with a hyper immune response beyond the BBB (known) that originated in the womb (known) and once started ran for months longer than it should (known). Add in that a similar sensitivity can start later in life from exposures to flu (known) or at middle age due to a natural increase with age (known). The observed reaction adds a dozen inflammatory chemicals to the brain environment (known) which lead to cell death (known) rather than killing cells outright and therefore more subtle. Most importantly from our standpoint is that these chemicals are themselves neuroactive and are neurotransmitters affecting behavior in major ways (known). Finally, all this chaos is tamped down or even eliminated by antibiotics, but only those known to have the ability to pass the BBB and counteract the chemical cocktail.

The reason I harped on that so much is that if a large part of our symptoms are the result of inflammation then PWP can go to the pharmacy tomorrow and choose a whole new way of relieving them just as you have done. Not five years - tomorrow! And not some high dollar side effect laden mess but instead some of the oldest and most studied and cheapest things on the shelf.

So. Is it possible for us to use our experiences in some way to prove or disprove any of this? To actually take a big step against PD that others can expand on?

I find it difficult to reconcile the reports of reduced symptoms following antibiotic treatment with the idea that a major part of the aetiology of PD is the death of dopaminergic neurons: if they were dead, how can the antibiotic lead to more dopamine?