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As a recent subsriber to the PD listserver I would like to introduce myself as Alan Pearce 50/8 from Perth in Western Australia ---------------------------------------------------------------- A few days back, Ivan Suzman outlined some of his symptoms, one of which is "I experience a kind of "rubberiness" at peak- or over- dose, where my neck is impelled to sway in soft, undulating, almost rhythmic oscillation." As far as I am aware this is classed as an 'abnormal involuntary movement'. About 80% of patients on full therapeutic levadopa doses for a year or longer will develop some abnormal movements. So this is a side effect which can be abolished by a decrease in the dose of levadopa. It is a case of your physician or neurologist adjusting dose to maximise benefit while minimizing side effects. Ivan then writes "It is a STRICTLY end-of-dose phenomenon. There is very rapid and forceful tremor of the arms. It can occur to me while sitting in a chair, while rising from a seated position, or while trying to walk. It is associated with back-of-the-neck sweating, and leaves me extremely immobilized, and precedes a deeper-than-usual off state, with very tense forearm muscles and great arm pain. It's as if I have depleted my reserves of dopamine, and maybe something else. I almost wonder if TWO chemicals are depleted, i.e., dopamine, which might in insufficient supply cause some sort of muscle tightness, or rigidity, and a chemical "x", which would allow smooth, rather than "cogwheeling" voluntary movement. Is "x" adrenaline?? This rapid end-of-dose arm shaking is so bad that for at least ten minutes, I can barely move my arms from the shoulders down, and meanwhile, I start pouring with perspiration." A simple model of smooth movement requires balanced components of dopamine (inhibition) and choline (excitation). So when the dopamine is depleted, muscle excitation is out of control. Many years ago, anticholinergic agents were used in the treatment of PD. These have largely been superceded by carbidopa as a decarboxylase inhibitor, which basically allows more of the levadopa to remain in the blood. Anticholinergic agents act by blunting the excitation process. Ivan, you do not say what your medication is, but I would suggest that you talk to your neurologist about reducing your levadopa (which I assume is in the form of Sinemet) and consider some type of anticholinergic drug. Always remember that more levadopa gets into your bloodstream if you take it 20 to 30 minutes before a meal. Take it with a cracker biscuit if you feel nauseous. Provided you maintain the recommended daily protein intake, you can increase the amount of levadopa which crosses into the brain by reducing protien consumption. A high protien diet increases the level of amino acids in the blood which restrict the amount of levadopa which can cross into the brain. Both of these diet strategies can allow you to reduce the dose of Sinemet for the same amount of movement control. It works for me. Instead of 1 to 2 hours ON time before, I now get 2 to 3+ hours from half tab of Sinemet 250/25. My apologies if there are any technical inaccuracies but this is my interpretation of the literature. Alan Pearce email: [log in to unmask] It's not really surprising that so many neurologists say to us PWP's that we seem to know more than they do. We experience symptoms of dose, overdose and end of dose that they rarely would see, unless they would be willing to spend hours watching us. Ivan Suzman