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Brian, Marty, et. al. Sorry to start a debate and then disappear, but it's been a long week at work and I didn't get around to my home e-mails. I'm tired so this will be short but hopefully it will keep everyone thinking for another week. If you revisit your system theory, you'll will recall that a stable control system must be both controllable and observable. Dopamine appears to affect our sensing function and thus impacts the observable part of the system. Acetylcholine actuates the muscles and therefore impacts the controllable part of the system. When we lose dopamine levels or we cannot properly use the dopamine, the system becomes unstable and we oscillate. We try to restablize by adding dopamine to retune the system. We try to detune the control path with a Pallidotomy. Let's assume for a moment that reduction in dopamine levels results in loss of gain in the feedbaaack loop. This means a larger change in position is required before the brain detects it and dampens the control of the actuated muscle. We add dopamine to restore this gain and restablize the loop. As the disease progresses the gain has a wider variation and is more difficult to stablize. Overmedication causes the gain to increase beyond normal levels. This says that a very small change in postion causes a large error signal. This will cause one muscle to be highly over damped, but the diametrically opposing muscle will be highly under damped. Depending upon the phase delay in the system we'll either see jerky movement (small phase delay) or large excursion movement (long phase delay). Of course, this theory relies on a summing node creating an error signal somewhere in the brain. I haven't found that yet. Also, the fact that we are really dealing with a multi-input multi-output system further complicates the problem. Disclaimer: This is my WAG at what is going on so noone should confuse this with fact. Phil Gesotti 49/46